ATL3 (atlastin GTPase 3) is a membrane-anchored GTPase that mediates GTP-dependent fusion of endoplasmic reticulum (ER) membranes, maintaining the continuous ER network 1. ATL3 facilitates three-way junction formation where ER tubules intersect through GTP-dependent homodimerization via its G-domain and 3HB regions, with subsequent GTP hydrolysis driving membrane fusion and homodimer disassembly 1. Beyond ER morphogenesis, ATL3 functions in ER-selective autophagy (reticulophagy), working in parallel with RTN3L and CALCOCO1 to target misfolded disease-causing proteins for lysosomal degradation at distinct ER-reticulophagy sites (ERPHS) 2. Under cellular stresses, ATL3 shapes tubulovesicular ER structures (ER tubular bodies) that mediate stress-induced, Golgi-independent secretion of trafficking-deficient proteins like ΔF508-CFTR and SARS-CoV-2 spike protein 1. Clinically, ATL3 mutations cause hereditary sensory neuropathy type 1F (HSN1F), characterized by distal sensory impairment, numbness, pain insensitivity, and muscle weakness in lower extremities 34. Only three ATL3 variants have been documented in HSN1F patients, with variable clinical presentations including hearing problems and gait disturbances 3. ATL3's role in maintaining ER homeostasis through both membrane fusion and selective autophagy suggests that neuropathic manifestations may result from impaired ER network integrity and proteostasis in sensory neurons.