DOCK1 (dedicator of cytokinesis 1) functions primarily as a guanine nucleotide exchange factor (GEF) that activates Rac small GTPases by exchanging bound GDP for free GTP, facilitating cytoskeletal rearrangements essential for cell migration and phagocytosis 1. The protein mediates critical cellular processes including epithelial and endothelial cell spreading, migration, and vitreous-induced retinal pigment epithelial cell functions through the DOCK1/ELMO1/Rac1 signaling axis 1. DOCK1 demonstrates significant disease relevance across multiple pathologies. In acute myeloid leukemia, high DOCK1 expression serves as an independent adverse prognostic factor, promoting cell survival through upregulation of Notch signaling pathways 2. Additionally, DOCK1 variants are associated with temporomandibular joint disorders and skeletal malocclusion 3. In cancer contexts, DOCK1 levels determine metformin treatment effectiveness in hepatocellular carcinoma, with synthetic lethality observed when DOCK1 is inhibited alongside metformin treatment 4. Clinically, DOCK1 represents a potential therapeutic target, as its inhibition sensitizes lung cancer cells to gefitinib through suppression of Akt signaling and vimentin phosphorylation 5. Furthermore, DOCK1 deficiency disrupts trophoblast function and pregnancy outcomes via the DUSP4-ERK pathway, contributing to recurrent spontaneous abortion 6.