DIPK2A (divergent protein kinase domain 2A) is a Golgi and late endosome/lysosome-localized kinase that regulates multiple cellular processes critical for cardiac and neurological function. Mechanistically, DIPK2A promotes autophagosome-lysosome fusion by binding to VAMP7B, thereby inhibiting its competition with functional VAMP7A for STX17 interaction and enhancing autophagic degradation of mitochondrial proteins 1. As a secreted paracrine factor (also termed HASF), DIPK2A stimulates cardiomyocyte proliferation through the PI3K-AKT-CDK7 signaling cascade 2. Additionally, DIPK2A modulates heparan sulfate proteoglycan (HSPG) homeostasis through Golgi trafficking; deletion of DIPK2A impairs α-synuclein fibril uptake by preventing cell surface binding, suggesting a role in neurodegeneration-related pathways 3. DIPK2A has been associated with multiple disease states: de novo mutations in DIPK2A occur more frequently than expected in non-syndromic cleft lip/palate 4, and genetic variants are linked to periodontal disease 5. The protein belongs to the FAM69/calcium-regulated kinase family implicated in neurological disorders 6, with involvement in PCOS pathophysiology through ceRNA networks 7.