GAN (gigaxonin) is a cytoskeletal component that functions as a substrate-specific adapter of E3 ubiquitin-protein ligase complexes, mediating ubiquitination and proteasomal degradation of target proteins. The gene plays a critical role in neurofilament architecture and neuronal maintenance. GAN controls the degradation of multiple targets including TBCB, MAP1B, and MAP1S, which are essential for proper microtubule cytoskeleton organization and neuronal survival. The protein localizes to the cytoplasm and cytosol, where it participates in proteasome-mediated ubiquitin-dependent protein catabolism through interaction with Cul3-RING ubiquitin ligase complexes. Mutations in GAN cause giant axonal neuropathy 1 (GAN1), an autosomal recessive disorder characterized by progressive neurological degeneration. This disease association underscores the critical importance of GAN-mediated protein degradation pathways for maintaining normal axonal structure and function. Loss of GAN function leads to accumulation of its substrates, disrupting neurofilament architecture and causing the characteristic pathology of giant axons observed in GAN1 patients.