DOCK3 is a guanine nucleotide exchange factor (GEF) predominantly expressed in neurons and skeletal muscle that regulates small GTPase-mediated signaling 1. As a GEF, DOCK3 activates RAC1 and other small GTPases to control actin cytoskeleton dynamics and cell adhesion 2. DOCK3 functions through multiple mechanisms: it interacts with HAUS7 to facilitate microtubule assembly and axon regeneration following nerve injury 3, and it directly binds NMDA receptors to promote their internalization and reduce excitotoxic damage in retinal ganglion cells 4. In skeletal muscle, DOCK3 regulates myogenic differentiation and glucose metabolism through interaction with SORBS1 5. Biallelic loss-of-function variants in DOCK3 cause a neurodevelopmental disorder characterized by intellectual disability, hypotonia, and ataxia 16. DOCK3 expression is dosage-sensitive; moderate reduction improves outcomes in Duchenne muscular dystrophy, while complete loss impairs muscle function 7. Additionally, DOCK3 dysregulation contributes to osteoporosis pathogenesis through Wnt signaling modulation 8. These findings identify DOCK3 as a critical regulator of neurological development, axonal regeneration, muscle health, and metabolic homeostasis, with therapeutic potential for neurodevelopmental disorders and muscle diseases.