DGKG encodes diacylglycerol kinase gamma (DGKγ), an ATP-dependent enzyme that catalyzes the phosphorylation of diacylglycerol (DAG) to phosphatidic acid (PA), functioning as a central lipid signaling switch 1. In the cerebellum, DGKG regulates protein kinase C gamma activity and controls Purkinje cell dendritic development and cerebellar motor coordination [UniProt]. Beyond its classical neurological role, DGKG has emerged as a context-dependent player in cancer progression. In hepatocellular carcinoma, endothelial DGKG is hypoxia-induced via HIF-1α and promotes tumor angiogenesis and immunosuppressive regulatory T-cell differentiation through the ZEB2/TGF-β1 axis 2. Similarly, a hypoxia-induced DGKG splice variant (DGKG-Δexon13) promotes glioblastoma proliferation, migration, and invasion 3. Conversely, in colorectal cancer, DGKG is epigenetically silenced through promoter hypermethylation in 51.8% of tumors, suggesting a tumor-suppressive role via Rac1 inhibition 4. DGKG has also been implicated in GABAergic interneuron maturation 5, cardiovascular disease pathways 6, and identified as an epilepsy-associated locus in genome-wide studies 7. These findings indicate DGKG exhibits tissue- and context-specific functions in both physiological development and malignant progression.