Targeting Novel Immune Therapeutic Intervention Points First-in-Class Treatments for Patients with Myopathies & Lung Diseases Novel I/O Target for Universal Backbone Therapy for Cancer Patients aTyr Pharma, Inc. August 2017 Exhibit 99.2

Forward-Looking Statements The following slides and any accompanying oral presentation contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and other federal securities laws.  The use of words such as “may,” “might,” “will,” “should,” “expect,” “plan,” “anticipate,” “believe,” “estimate,” “project,” “intend,” “future,” “potential,” “opportunity,” or “continue,” and other similar expressions are intended to identify forward-looking statements.  For example, all statements we make regarding the potential therapeutic benefits of Physiocrines and our product candidates, including Resolaris™, our iMod.Fc program and Project ORCA, the ability to successfully advance our pipeline or product candidates, the timing within which we expect to initiate, receive and report data from, and complete our planned clinical trials, and our ability to receive regulatory approvals for, and commercialize, our product candidates, our ability to identify and discover additional product candidates, our projected cash expenditures, and the ability of our intellectual property portfolio to provide protection are forward-looking statements. All forward-looking statements are based on estimates and assumptions by our management that, although we believe to be reasonable, are inherently uncertain. All forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those that we expected. These risks, uncertainties and other factors are more fully described in our filings with the U.S. Securities and Exchange Commission, including our Quarterly Report on Form 10-Q, our Annual Report on Form 10-K and in our other filings. The forward-looking statements in this presentation speak only as of the date of this presentation and neither we nor any other person assume responsibility for the accuracy and completeness of any forward-looking statement. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law. We own various U.S. federal trademark applications and unregistered trademarks, including our company name, Resolaris™. All other trademarks or trade names referred to in this presentation are the property of their respective owners. Solely for convenience, the trademarks and trade names in this presentation are referred to without the symbols ® and ™, but such references should not be construed as any indicator that their respective owners will not assert, to the fullest extent under applicable law, their rights thereto.

LIFE Candidate Pipeline All programs currently wholly-owned Resokine Agonist Platform Preclinical Phase 1 Phase 2 Phase 3 Rare Muscular Dystrophies Resolaris Program (ATYR 1940)* Interstitial Lung Diseases iMod.Fc Program (ATYR 1923) Resolaris Program (ATYR 1940) Resokine Antagonist Platform Preclinical Phase 1 Phase 2 Phase 3 Various Cancers Project ORCA Resokine Pathway Hypothesis: A homeostatic pathway that controls the set point of key cells in the immune system. (Reso for resolution; Kine for activity) *Future development of Resolaris for Rare Muscular Dystrophies gated to a partnership iMod.Fc to enter clinic in 2017 IND candidate to be selected in 2017

Evolved from Cellular Homeostasis Genes over 400 Million Years Tapping the Power of the Resokine Pathway

Resokine Pathway: Evidence For A New Immunological Pathway in Humans: Resokine Disrupting the pathway promotes T-cell invasion Homeostasis Imbalance (↑ Immune cell invasion/activity) Diseased Muscle Diseased Lung Healthy muscle Healthy lung 100% (18 of 18) anti-synthetase syndrome patients tested positive for antibodies for Resokine iMod domain Modulates Immune System Antibodies Antagonize Modulation Unpublished data from aTyr and collaborator Statistics: Mann-Whitney test, p-value < 0.0001 Free Resokine Levels in Healthy Volunteers (n=117) 0/117 Healthy Volunteers with Undetectable Levels of Free Resokine Free Resokine Levels in Anti-Synthetase Syndrome Patients (n=52) 36/52 Patients with Undetectable Levels of Free Resokine p-value <0.0001

Resokine Levels Influence Tolerance and Immunity Resokine pathway as a set point modulator of immune engagement Adapted from graphic from Chen et al 2017 Tolerance Suppression Immunity Inflammation Immune Cell Population n

Resokine Hypothesis in Immune Invaded Tissues: Damage Signals Exceed Resokine Ability to Resolve Immune Engagement Adapted from graphic from Chen et al 2017 Tolerance Suppression Immunity Inflammation Immune Cell Population n Muscle Disease Lung Disease

Resokine Hypothesis in Cancer: Higher than Normal Resokine Adapted from graphic from Chen et al 2017 Tolerance Suppression Immunity Inflammation Immune Cell Population n Tumor Tissue

Boivin et al., Lab Invest., 2009 Chen et al., Immunity, 2013 MOA Hypothesis: T Cells Release Granzyme B That Promotes Cell Death & Local Tissue Damage Muscle Disease Lung Disease Tumor Tissue Promotes Cell Death T cell (Activated) T cell (Less Activated) T cell (Activated/ No Resokine) Resokine bound

Resokine Inhibits Granzyme B Release From Activated Human T Cells Key mediator of T cell cytotoxicity Resokine (pM) Human T Cell Granzyme B Release Post Activation vehicle 30,000 Stimulated Potential For More Tissue Damage **** p < 0.0001 Granzyme B Promotes Cell Death Note: Common with human donors and T cell assays to have variability

Effector functions at levels closer to a resting T cell Stimulatory pathways at levels closer to a resting T cell Resokine Agonists Change T Cell Phenotype Unique MOA to orchestrate immune homeostasis in activated T cells Shifts trafficking & residence closer to a resting T cell T cell (Less activated) Acts predominantly on CD4 & CD8 (activated only) T cell (Activated; No Resokine) Resokine

Harnessing New Immunological Insights Across 3 Therapeutic Areas, 3 Therapeutic Modalities TPP = Target Product Profile ILD = Interstitial Lung Disease ORCA = Orchestrating Resokine Complete Antagonism Resolaris “Native Agonist” to Resokine pathway May promote tissue homeostasis in muscle & lung No observed signs of immunosuppression; Signals of potential improved muscle function iMod.Fc “Engineered Agonist” Splice variant of Resokine fused to Fc of antibody May promote tissue homeostasis in lung Fc reduces clearance; allowing for potential TPP of monthly dosing ORCA “Antagonist” Antibody to Resokine pathway Potential to Disrupt tumor homeostasis Preclinical tumor activity; Pathway appears upregulated in cancer Cooling Down the Immune System Heating Up the Immune System

Harnessing the Resokine Pathway to Treat Multiple Rare Muscle Diseases Resolaris Program

Rare Myopathies Have an Immune Component Chronic damage, homeostasis disrupted Genetic Mutation Inappropriate proteins in muscle Mutated dysferlin proteins in muscle Mutated dystrophin proteins in muscle FSHD LGMD2B DMD Aberrant Protein Expression Localized T Cell Invasion/Engagement Untapped therapeutic intervention point Frisullo et al., J. Clin. Immunol., 2011. Gallardo et al. Neurology, 2001. Flanigan et al. Human Gene Therapy, 2013. FSHD = Facioscapulohumeral Muscular Dystrophy. LGMD2B = Limb Girdle Muscular Dystrophy 2B. DMD = Duchenne Muscular Dystrophy. Potential to link genotype to specific T cell phenotype All debilitating diseases with little or no therapeutic treatments While maintaining muscle biology

Resolaris Program Snapshot Patients Rare Myopthies with an Immune Component Therapeutic concept Upregulate naturally occurring homeostatic pathway involving immune cells Target Resokine pathway: activated T-cell Rationale Functional knockout in humans & rodents results in increased muscle damage Molecular entity 57.4kD monomer (recombinant human Resokine slightly truncated) Affinity In vitro cell assay (human T cells) EC50 ≤ 100 pM Human active dose 3.0 mg/kg (weekly or bi-weekly) Human safety profile 44 patients have received Resolaris for a total drug exposure of 204 patient months Generally well-tolerated; low-level anti-drug antibody signals did not result in clinical symptoms; some transient infusion related reactions observed No observed signs of general immunosuppression 12 patients have received at least 6 months of Resolaris with no significant trends of worsening in either muscle function or quality of life assessments Clinical activity Muscle function signals: Adult LGMD2B, Early onset FSHD > Adult FSHD Overall patients not feeling worse as measured by quality of life questionnaire Clinical development plans Conduct large randomized controlled trial (RCT) in rare muscular dystrophy (commence post partnership)

Resolaris Clinical Data from Three Phase 1/2a Clinical Trials Signals of clinical activity (improved muscle function) in patients n = 4 n = 2 n = 4 n = 8 n = 9 Overall Mean MMT Change Week 14 by Dose Group FSHD & LGMD2B Patients From 002, 003, 004 Trials Mean Change from baseline (%) Decrease Muscle Function Increase Muscle Function n = 6 002 Adult FSHD 3.0 mg/kg Placebo-controlled 004 Adult FSHD 1.0 mg/kg Open-label 004 Adult LGMD 3.0 mg/kg Open-label 003 E.O.FSHD 3.0 mg/kg Open-label 004 Adult FSHD 3.0 mg/kg Open-label MMT = Manual Muscle Testing a validated assessment of muscle function/strength in 14 muscle groups E.O. = Early Onset 002 Adult FSHD Placebo Placebo control 50% to 78% of patients in Resolaris dose groups had increased MMT scores

Lung Physiocrine Engineered to Treat Multiple Pulmonary Diseases iMod.Fc Program

Interstitial Lung Disease Severe tissue remodeling Resokine Promotes Lung Homeostasis Epithelial damage IL-13, TGFβ, TNF, IL-1β Resokine Therapy to “Cool Down” Immune System Pharmacologic restoration of tissue homeostasis and resolution of immune engagement Natural restoration of tissue homeostasis and resolution of immune engagement Perturbation Injury Infection Genetic Exacerbation Fibrocytes EMT Fibroblasts Circulation Natural Resokine levels IL-1β, TNF, IFNɣ T Cell Neutrophil Macrophage Mast Cell Excess deposition of extracellular matrix (ECM) iMod Resokine Granzyme B

Connective Tissue Diseases (CTDs) Occult CTD + Serologies Idiopathic Pulmonary Fibrosis (IPF) Constant Immune Engagement: Acute & Chronic Sarcoidosis Chronic Hypersensitivity Pneumonia Non-Specific Interstitial Pneumonia Level of Fibrosis Interstitial Lung Diseases Shared Immune Engagement Significant and persistent immune engagement provoking fibrosis Interstitial Lung Diseases (ILDs) span the spectrum in terms of level of fibrosis; but all share persistent immune engagement Slide adapted from Dr. Steven Nathan, Medical Director, Advanced Lung Disease & Transplant Program at Inova Fairfax Hospital, Falls Church, VA

Pathophysiological Role of T Cells in ILD Idiopathic Pulmonary Fibrosis Hypersensitivity Pneumonitis Sarcoidosis Prasse et al. Clin Exp Immunol 2000 Daniil et al. Resp Research 2005 Arranz, et al. Eur Resp J 2016 T Cells Correlated with Negative Outcomes Percentage of lymphocytes in pulmonary lavage independently associated with survival Sarcoidosis patients Healthy volunteers TLC= Total Lung Capacity FVC = Forced Vital Capacity *slow and rapid progressors Elevated T Cell Activity in ILDs Healthy control Non-active sarcoidosis Active sarcoidosis Balestro et al. PLOS ONE. 2016 Barrera et al. Am J Respir Crit Care Med 2007 Minshall et al. Eur Resp J 1997 Probability of Survival # at risk Time (years)

*The Ashcroft scale for the evaluation of bleomycin-induced lung fibrosis is the analysis of stained histological samples by visual assessment **Bleomycin mouse model abstract presented as a poster at the American Thoracic Society in May 2017 Improvement in Ashcroft Score (%)* TGF β Ab 3mg/kg IP QOD D0-D 21 Pirfenidone 100 mg/kg PO BID D8-D 21 iMod.Fc 0.4 mg/kg IV mg/kg D8, D15 33 Total drug (mg/kg) 2,800 0.8 Outperformed Pirfenidone (SOC for IPF) and TGFβ Ab (Fibrosis pathway blocker) in the bleomycin IPF model at lower and less frequent dosing** iMod.Fc Outperforms Current Treatment Established rodent model for idiopathic pulmonary fibrosis (IPF)

***P ≤ 0.001; ****P < 0.0001; ns = not significant Respiratory Minute Volume = amount of air inhaled/exhaled/min Nintedanib dosed daily iMod.Fc Returns Breathing to Normal Respiratory Minute Volume iMod.Fc iMod.Fc iMod.Fc outperformed Nintedanib (SOC for IPF) in the respiratory mouse model at lower and less frequent dosing

iMod.Fc Program Snapshot Patients Interstitial Lung Diseases, including IPF Therapeutic concept Upregulate naturally occurring homeostatic pathway involving immune cells Target Resokine pathway: activated T-cell Rationale Functional knockout in humans & rodents results in lung damage Molecular entity 64.5kD: covalent dimer (native human Resokine iMod + Fc AA sequence) Affinity In vitro cell assay (human T cells) EC50 ≤ 100pM Proposed human dosing 0.03 mg/kg up to 5.0 mg/kg Target administration Monthly dosing (IV infusion) Clinical development plans Conduct Phase 1/2a single and multiple ascending dose trial in healthy volunteers (commence 2017) and patients with interstitial lung disease (commence 1H 2018)

Phase 2a Potential Patient Analysis: BALF Imaging: HRCT, PET Disease Biomarkers: ACE, IL-2R, Neopterin, Resokine PD Assay iMod.Fc Phase 1/2a Program Current Plan Program Overview (Final trial designs subject to approval of regulatory authorities) Randomized, Double-Blind, Placebo-Controlled Studies to Investigate the Safety, Tolerability, Immunogenicity, Pharmacokinetics and Pharmacodynamics of Intravenous ATYR1923 (iMod.Fc) in Healthy Volunteers and Patients with Interstitial Lung Disease. Phase 1 - Healthy Volunteers: Approximately 36 subjects Single study drug infusion Starting at 0.03 mg/kg, increasing at half-log, up to potentially 5.0 mg/kg Initiation – first subject expected to be dosed in the second half of 2017 Data expected in first half of 2018 Phase 2a: – Interstitial Lung Disease Patients: First patient expected to be dosed mid-2018; with potential data read-outs within 6 months of trial initiation BALF = Bronchoalveolar Lavage Fluid analysis PET = Positron Emission Tomography scan HRCT = High-Resolution Computed Tomography ACE = Angiotensin Converting Enzyme

By Hijacking a 400 Million Year Old Pathway, Resokine Cancer Promoting Tumor Homeostasis

Resokine: Potential Key Regulator of Tissue & Tumor Homeostasis Cancer homeostasis follows homeostasis evolution tRNA Synthetase Physiocrines *Resokine, CTLA-4, PD-1 timeline for when >70% sequence identity Guo et al. Nature 2010; Science 2017; Science 2007; Nature 2002; Nature 2010; Genome Research 2000 Tumor Growth Mirrors LIFE Evolution: Cell with mutation Dysplasia Hyperplasia In situ cancer Invasive cancer Years Ago: ~3.5 billion ~450m ~360m ~75m ~25m ~300k Cellular Homeostasis Complex Tissue Homeostasis (mammalian immune system) Resokine* CTLA-4 PD-1

B Project ORCA: Resokine Antagonists Activating T Cells “Turning Up the Heat” To Disrupt Tumor Homeostasis

Higher Resokine Levels in Tumors: Colder Immune System at the Tumor Adapted from graphic from Chen et al 2017 Tolerance Suppression Immunity Inflammation Immune Cell Population n 2 Increases the local tumor requirement for immune cell activation/ engagement 1 Tumor “highjacks” the primal homeostatic pathway 4 Increased likelihood of immuno-shielding metastatic tumor cells 3 Increased Pathway levels in circulation from diffusion Resokine Proteins

Setting Lower Resokine Levels in Cancer Patients in Tumors: Hotter Immune System at the Tumor Adapted from graphic from Chen et al 2017 Tolerance Suppression Immunity Inflammation Immune Cell Population n 1 Potential to therapeutically disrupt cancer homeostasis 2 Target Resokine Pathway 3 With an antibody

ORCA: Development Highlights & Status Development Highlights Status Resokine over expressed in all cancers tested to date Over 10 tumor types tested; >300 patient samples tested; ≥95% of patients tested positive for Resokine Human evidence of Ab blockade; changes T cell behavior Anti-synthetase syndrome patients Key blocking epitope Out of multitude of Resokine epitopes Tested Resokine Abs in multiple mouse syngeneic tumor models Outperformed checkpoint inhibitors (e.g. Abs to PD-1, PD-L1, and CTLA-4) in various animal models Tested Resokine Abs in combination Efficacy potential as monotherapy and Resokine Abs with checkpoint inhibitors (based on tumor model data) Resokine Ab assay development & “Druggability” Resokine Abs shown to knock-out Resokine pathway Biomarker identified and tested Liquid biopsy: correlates with tumor volume and efficacy Resokine antibody selection On track to declare an IND candidate by end of 2017 Publications/preclinical presentations Throughout 2018 Phase 1 2019

Building a New Class of Therapeutics For Patients Foundation for the Future

LIFE Leaders Andrea Cubitt, Ph.D. VP, Product Protection John Blake, CPA SVP, Finance Sanjay Shukla, M.D. Chief Medical Officer Holly D. Chrzanowski VP, Enterprise Talent and Organization Ashraf Amanullah, Ph.D. VP, Manufacturing John Mendlein, Ph.D. Chief Executive Officer Sanuj Ravindran, M.D. Chief Business Officer David King, Ph.D. SVP, Research Grove Matsuoka SVP, Product Programs and Planning Nancy Krueger VP, Legal Affairs

LIFE Corporate Goals and Financial Update Corporate Goals Advance Pipeline with Two Molecules in the Clinic iMod.Fc scheduled to commence Phase 1 in 2017 Declare 3rd IND Candidate ORCA on track to declare an IND candidate in 2017 Partner One or More Wholly-Owned Programs Active discussions ongoing (Resolaris/iMod.Fc/ORCA) Financial Update $57.2M cash and investments as of 6/30/2017 Announced Private Placement on 8/28/17 with $45.8M in gross proceeds