GDAP1 is a mitochondrial outer membrane protein that regulates the mitochondrial network by promoting mitochondrial fission 1. As an atypical glutathione S-transferase, GDAP1 functions in multiple cellular processes including mitochondrial dynamics, autophagy, and membrane contact sites between mitochondria and lysosomes 1. GDAP1 participates in basal autophagy and interacts with lysosomal machinery, including the novel interaction with LAMP-1 to mediate mitochondria-lysosome membrane contacts critical for lysosomal maturation 1. GDAP1 also contributes to cellular glutathione homeostasis and calcium regulation. Mutations in GDAP1 cause multiple forms of Charcot-Marie-Tooth (CMT) disease, including axonal type 2K, demyelinating type 4A, and recessive intermediate forms 23. CMT-GDAP1 disease manifests as early-onset, progressive distal-muscle wasting and axonal degeneration 4. GDAP1 mutations account for a small percentage of CMT cases overall but are significant contributors to recessive CMT subtypes 5. GDAP1 deficiency impairs mitochondrial networks, reduces mitochondria-lysosome contacts, and decreases cellular glutathione levels, underlying the primary pathophysiology of CMT 1. Additionally, GDAP1 variants have been identified in genome-wide association studies for endometriosis and type 2 diabetes, suggesting broader physiological roles 67.