DOCK10 is a guanine nucleotide-exchange factor (GEF) that activates the small Rho GTPases CDC42 and RAC1 by promoting GDP-to-GTP exchange 1. The gene exhibits cell-type-specific expression through alternative splicing, producing two main isoforms—DOCK10.1 enriched in T cells and DOCK10.2 enriched in B cells 2. Both isoforms are upregulated by interleukin-4 signaling in B cells 3. Mechanistically, DOCK10 regulates multiple cellular processes through CDC42 and RAC1 activation. In epithelial cells, DOCK10-dependent Rac1 activation promotes epithelial-to-mesenchymal transition via FoxO1 activation 4, while CDC42 activation induces filopodia formation and membrane protrusions 1. The protein localizes to both cytoplasmic and nuclear compartments 3. Clinically, DOCK10 has emerged as a significant player in pancreatic neuroendocrine tumors and immune dysfunction. DOCK10 is selectively overexpressed in insulin-secreting insulinomas, and DOCK10 knockdown impairs glucose-stimulated insulin secretion; CDC42 inhibition reduces insulin hypersecretion and improves survival in xenograft models, suggesting therapeutic potential 5. Additionally, DOCK10 has been identified as an aging-related hub gene associated with sepsis pathogenesis and prognosis 6, and serves as a novel marker gene for beta cells in pancreatic islets 7.