CRMP1 (collapsin response mediator protein 1) is a cytoplasmic protein essential for neuronal development and axon guidance. Mechanistically, CRMP1 functions downstream of semaphorin 3A (SEMA3A) signaling to promote filamin A dissociation from F-actin, enabling actin cytoskeleton rearrangement and growth cone collapse 1. CRMP1 also couples with sodium channel Nav1.7 to mediate SEMA3A-induced retrograde axonal transport 2. Beyond development, CRMP1 regulates cell migration and proliferation, functioning as an invasion suppressor in medulloblastoma 3. Clinically, CRMP1 dysfunction is implicated in multiple neurological and psychiatric conditions. Heterozygous de novo variants in CRMP1 cause a neurodevelopmental disorder characterized by muscular hypotonia, intellectual disability, and autism spectrum disorder through disrupted protein oligomerization 4. In amyotrophic lateral sclerosis (ALS), elevated phosphorylation of CRMP1 at Ser522 contributes to motor neuron degeneration; blocking this phosphorylation ameliorates motor function and preserves neuromuscular junctions in ALS models 5. CRMP1 is also associated with schizophrenia, showing increased insoluble protein accumulation in patient brains and genetic association with anhedonia 6. Recent evidence links CRMP1 to bipolar disorder pathogenesis 7 and identifies it as a genetic modifier of Ellis-van Creveld syndrome severity 8. Upregulating developmentally downregulated CRMP1 promotes axon regeneration and neuronal survival after CNS injury 9.