Audentes Corporate Overview September 27, 2017 Exhibit 99.4

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Multi-product pipeline based on focused selection criteria Proven leadership team with significant experience Internal cGMP manufacturing provides core strategic advantage Targeting indications with limited or no treatment options Preliminary clinical data from lead programs expected end of 2017 Audentes Therapeutics A clinical-stage biotechnology company developing gene therapy products to treat serious, life-threatening rare diseases

Experienced and Passionate Team Audentes Therapeutics 117 employees based in the San Francisco Bay Area as of June 30, 2017 Matthew Patterson President and Chief Executive Officer Natalie Holles Senior VP and Chief Operating Officer Thomas Soloway Senior VP and Chief Financial Officer Suyash Prasad, M.D. Senior VP and Chief Medical Officer John Gray, Ph.D. Senior VP and Chief Scientific Officer Mary Newman Senior VP, Regulatory Affairs David Nagler Senior VP, Human Resources and Corporate Affairs

Robust Pipeline AT132 AT342 AT307 AT982 Applying world-class AAV science to monogenic diseases with high potential for transformative clinical benefits IndicationStage of DevelopmentCommercial RightsProof-of-ConceptIND EnablingPhase 1/2XLMTMCrigler-Najjar SyndromePompe DiseaseCASQ2-CPVT

Audentes Internal cGMP Manufacturing Leadership Position in AAV Manufacturing Superior control over timelines, cost and IP Enables rapid addition of new programs 38,000 square feet in South San Francisco 2 x 500L scale ongoing to supply clinical trials In-house QC lab for critical release assays Additional capacity (~5,000L) possible in existing lease footprint Facility and process designed to meet global regulatory requirements and support commercialization Designed for seamless transition from IND enabling studies through commercial launch Advantages of internal cGMP manufacturing Commercial readiness Large-scale cGMP capacity Natural host for AAV Significant regulatory history with HEK293 Industrial scale serum-free suspension culture system Mammalian cell-based production platform

AT132 X-linked myotubular myopathy

XLMTM A Fatal Disease with no Treatment Options Significant impairment of respiratory and neuromuscular function Estimated 50% mortality by 18 months Incidence: 1 in 50K newborn males AAV8 effectively penetrates skeletal muscle Muscle tissue is otherwise reasonably healthy and exhibits no dystrophic or inflammatory change MTM1 gene encodes myotubularin, an enzyme required for normal development and function of skeletal muscle Respiratory function measured by maximum inspiratory pressure (MIP) Neuromuscular function as measured by validated scales Muscle biopsy Hnia, Beggs, et al. J Clin Invest. 2011, Joshua Frase Foundation. McEntagart, 2002 Serious, life-threatening rare disease Target for AAV gene therapy Clear clinical measures Monogenic, well-understood biology

Normal (n=13) XLMTM (n=2) XLMTM+AT132 (n=3) 0 50 100 150 0 50 100 Percent survival Single injection of 2 x 1014 vg/kg AT132 in 3 week and 5 week old MTM1 KO mice M. K. Childers et al., Sci Transl Med, 2014; Buj-Bello, et al. Human Molecular Genetics, 2008; Note: vector dosing numbers have been adjusted from publication as a result of improvements in titration methodology Normal Mice + Placebo MTM + Placebo MTM + AT132 Prototype P ≤ 0.001 P ≤ 0.001 XLMTM Canine Model MTM1 KO Mouse Model Weeks of age Untreated MTM1 KO Mice + Placebo, n = 10 MTM1 KO + AT132 (5 weeks), n = 11 MTM1 KO + AT132 (3 weeks), n = 8 Normal Mice + Placebo, n = 10 Single injection of 2 x 1014 vg/kg AT132 A Single Treatment with AT132 Results In Dramatic Improvement & Survival in XLMTM Mouse and Dog Models P ≤ 0.001

*Dogs 3, 4 and 5, the three dogs treated in the proof-of-concept canine study, achieved a statistically significant improvement in survival. Treatment with AT132 Results in Dramatic Improvement and Survival in XLMTM Dogs

AT132 Clinical Development Program INCEPTUS Prospective Natural History Run-in Study in XLMTM Patients N≈16 Longitudinal baseline and within-patient control for ASPIRO Facilitates enrollment in and operational aspects of ASPIRO ASPIRO A Phase 1/2 Gene Therapy Study in XLMTM Patients N=12 Assessment of safety and tolerability and preliminary efficacy Focus on neuromuscular & respiratory measurements RECENSUS A Medical Chart Review of Patients with XLMTM N=112 Characterize aspects of the disease and medical management of XLMTM Identify potential outcome measures for ASPIRO Initial presentation Q1:17; Publication planned Q4:17 Preliminary data available from on-going study First patient dosed Q3:17; Prelim. data expected YE:17 Orphan Drug Designation received from FDA and EMA Rare Pediatric Disease and Fast Track designations granted

INCEPTUS: Key Findings Prospectively collected natural history data confirm poor clinical outcomes of children living with XLMTM (n=18) Key Findings Data High frequency of life- threatening events 89 Adverse Events, 23 Serious Adverse Events, 1 patient death Approximately 100 cumulative hospitalization days in patients with SAEs, primarily due to respiratory complications Severely impaired motor development and function CHOP-INTEND and MFM-20 functional scores well below normal No patient has achieved rolling, standing or walking milestones Highly compromised respiratory function Majority of patients require permanent 24/7 ventilation All patients score significantly below normal on key respiratory measures

CHOP-INTEND Scores All patients have severely impaired motor abilities and have missed all major gross motor milestones (rolling, standing, walking) Note: Interim data as of September 14, 2017 Age Range: 8 mos. to 4 yrs.

MFM-20 Scores All patients scoring well below normal on neuromuscular function Normal score in healthy children over 2 years of age Note: Interim data as of September 14, 2017 Age Range: 8 mos. to 4 yrs.

Ventilator Dependence Within the Previous 24 Hours Majority of patients require continuous (24/7) ventilator support Invasive Ventilation N=13/18 Non-Invasive Respiratory Support (Bi-PAP) N=5/18 Note: Interim data as of September 14, 2017

Respiratory Sprinting Test – Median Time Off Ventilator Most patients cannot tolerate more than 10 min off ventilator Note: Only patients on invasive ventilator support undergo a sprinting test Note: Interim data as of September 14, 2017

Maximum Inspiratory Pressures Respiratory strength of patients as measured by maximum inspiratory pressure is consistently well below normal levels Normal minimal pressures in healthy children Note: Interim data as of September 14, 2017

ASPIRO Phase 1/2 Clinical Study Baseline AT132 Administration Subjects from INCEPTUS Weeks 1 – 4 Prednisolone Weeks 5–9 Taper Extension study Baseline Assessments Neuromuscular Respiratory Biopsy Assessments Neuromuscular Respiratory Biopsy Assessments Neuromuscular Respiratory Biopsy Assessments Neuromuscular Respiratory 3 mos. 6 mos. 12 mos. Inclusion Criteria Subject is male <5 yrs old, or enrolled in INCEPTUS Genetically confirmed XLMTM Requires ventilator support Key Efficacy Assessments Neuromuscular CHOP INTEND MFM-20 Bayley III Muscle biopsy Respiratory Ventilator use Respiratory sprinting Max Inspiratory Pressure (MIP) Design N=12, roll-over from INCEPTUS 3 ascending-dose cohorts (3 active plus a delayed treatment concurrent control) Doses: 1x1014, 3x1014, 5x1014 vg/kg Open-label, Ascending-Dose, Safety and Preliminary Efficacy Study

AT342 Crigler-Najjar syndrome

Crigler-Najjar Syndrome A Rare Disease that Leads to Neurological Damage and Death Significant bilirubin accumulation that can lead to irreversible neurological damage and death Current treatments: > 12 hours/day of phototherapy, liver transplant Estimated incidence of 1 in 1 million newborns AAV8 effectively penetrates the liver In the majority of patients, liver tissue is otherwise healthy UGT1A1 gene encodes enzyme required for bilirubin metabolism and excretion Serum bilirubin Time on phototherapy Serious, life-threatening rare disease Target for AAV gene therapy Clear clinical measures Monogenic, well-understood biology Bortolussi et. al, Human Gene Therapy, 2014; Orphanet.com

AT342 Rapidly Reduces Bilirubin Levels in Crigler-Najjar Mouse Model A single tail vein injection of AT342 in a knockout mouse model rapidly reduced and normalized bilirubin levels for the duration of the study Previously published study with AAV8-UGT1A1 in a knockout mouse shows durable effect out to 17 months Total Bilirubin Levels (mg/dL) Days 1.5 x 1010 vg/kg (n=5) 1.5 x 1011 vg/kg (n=5) 1.5 x 1012 vg/kg (n=5) 1.5 x 1013 vg/kg (n=5) Vehicle Control Bortolussi et. al, Human Gene Therapy

AT342 Development Program LUSTRO Prospective Natural History Run-in Study in Crigler-Najjar Patients (N=16 to 18) Longitudinal baseline and within-patient control for VALENS Facilitates enrollment in and operational aspects of VALENS VALENS A Phase 1/2 Gene Therapy Study in Crigler-Najjar Patients N=12 Assessment of safety and tolerability and preliminary efficacy Focus on serum bilirubin & phototherapy use Preliminary data available Q4:17 Plan to initiate VALENS Q4:17; Prelim. data expected YE:17 Orphan Drug Designation received from FDA and EMA

VALENS Phase 1/2 Clinical Study Open-Label, Ascending-Dose, Safety & Preliminary Efficacy Study Assessments Initial assessments Liver biopsy Weeks 5–9 Taper Weeks 13 – 17 Weaning Weeks 1 – 4 Prednisolone Assessments ∆ Bilirubin Weeks 1 – 12 Normal prescribed phototherapy dose Assessments Liver biopsy AT342 Administration Subjects from LUSTRO Assessments ∆ Bilirubin ∆ Phototherapy Extension study Design N=12, roll-over from LUSTRO 3 ascending-dose cohorts (3 active plus a delayed treatment concurrent control) Doses: 1.5x1012, 6.0x1012, 1.5x1013 vg/kg Key Assessments ∆ bilirubin from baseline (BL) to 12 wks. ∆ bilirubin from BL to 18 wks. ∆ phototherapy (PT) from BL to 18 wks. Successful weaning from PT Liver biopsy Inclusion Criteria Genetically confirmed Crigler-Najjar ≥ 1 year of age Subject receives daily phototherapy for ≥6 hours within a 24 hour period Baseline Week 12 Week 18 Week 24

AT982 Pompe disease

Pompe Disease A Rare, Severe, Progressive Neuromuscular Disease Severe muscle weakness, respiratory failure, and in infants, increased cardiac mass and heart failure Spectrum of disease from severe (infantile/early-onset) to more attenuated (juvenile/late-onset) Estimated incidence of 1 in 40K Efficacy of ERT limited by poor cellular uptake, no neuronal exposure, and immune reaction to exogenous GAA Published animal Proof-of-Concept utilizing both muscle- and liver-directed AAV approaches Gene encodes lysosomal enzyme acid alpha-glucosidase (GAA), deficiency leads to accumulation of lysosomal glycogen Respiratory function by MIP Neuromuscular function as measured by validated scales Muscle biopsy Serious, life-threatening rare disease Target for AAV gene therapy Clear clinical measures Monogenic, well-understood biology Lipinksi, Shawn. Molecular Genetics and Metabolism, 2012; Lacana, et al., Amer. J. Medical Genetics, 2012; International Pompe Association, Pompe Community and United Pompe Foundation

AT982 Development Path to planned phase 1/2 clinical study Activity Overview and Achievements Preclinical studies Proof of concept established in murine model Comprehensive construct selection study ongoing - Muscle, neuronal and liver-directed vectors, AAV8 & AAV9 Functional, biochemical, immunological endpoints Regulatory Orphan Drug Designation granted by FDA and EMA IND planned H1:18 Chemistry, Mfg. & Controls (CMC) Leverages existing AT132 and AT342 process and methods Clinical supply manufacturing preparations underway Clinical development Phase 1/2 study planned H2:18

AT307 Catecholaminergic polymorphic ventricular tachycardia (CPVT)

CASQ2-CPVT A Life-Threatening Inherited Arrhythmia Ventricular arrhythmias and sudden death in response to stress and/or exercise Prevalence estimated at > 6,000 in addressable markets with mortality of 30-50% by age 30 AAV9 vector capsid effectively penetrates heart tissue Heart tissue is otherwise healthy Autosomal recessive form (CASQ2) : gene encodes calsequestrin 2, essential for normal calcium homeostasis in cardiac myocytes Electrocardiogram during exercise stress test Episodes of VT and/or syncope Serious, life-threatening rare disease Target for AAV gene therapy Clear clinical measures Monogenic, well-understood biology Cerrone et al., Circulation Cardiovascular Genetics, 2012; Napolitano et al., Circulation, 2012; Priori et al. Europace, 2013; GeneReviews: http://www.ncbi.nlm.nih.gov/books/NBK1289/

A single administration of an AT307 prototype achieved: Near normal levels of CASQ2 protein expression Reduction in pre-arrhythmic events and ventricular tachycardia to normal levels in both newborn and adult mice Denegri et al., Circulation, 2014 Newborn Mice P < 0.001 P < 0.001 P < 0.001 P < 0.001 P < 0.001 P < 0.05 Adult Mice P < 0.001 P < 0.05 AT307 Prototype Prevents VT in Newborn Mice and Reverses VT in Adult Mice

Financial Overview & Summary

Jun. 30, 2017 cash, equivalents & short-term investments: $145M Funded to achieve key value inflection milestones: XLMTM: Interim results from the ASPIRO study Crigler-Najjar: Interim results from the planned VALENS study Pompe disease: File IND, initiate Phase 1/2 study for systemic administration of AT982 CASQ2-CPVT: File IND and initiate Phase 1/2 study of AT307 Q1:17 (Unaudited) Q2:17 (Unaudited) R&D Expense $14.3M $18.8 G&A Expense $ 3.9M $4.1 Loss from Ops. $(18.2M) $(22.8) Financial Overview

Audentes Highlights Treating devastating diseases with high unmet medical need Potential for transformational disease impact Compelling Pipeline AAV Gene Therapy Leadership Team with significant rare disease and gene therapy expertise Robust internal research, analytical and large-scale cGMP manufacturing capabilities Catalysts Catalysts Preliminary AT132 clinical data planned Q4:17 Preliminary AT342 clinical data planned Q4:17 Plan to file AT307 IND year-end 2017 Plan to file AT982 systemic administration IND H1:18 US and EU Orphan Drug Designation for all programs Establish large-scale cGMP manufacturing AT132 first patient dosed AT342 IND active ✓ ❐ ✓ ❐ ✓ ❐ ✓ ❐ ❐ ❐ ❐ ❐

Audentes Corporate Overview September 27, 2017