ITPKA (inositol-trisphosphate 3-kinase A) is a dual-function enzyme that catalyzes phosphorylation of inositol 1,4,5-trisphosphate (InsP3) into inositol 1,3,4,5-tetrakisphosphate, regulating calcium homeostasis [UniProt]. Beyond its canonical enzymatic role, ITPKA possesses actin bundling activity 1. The protein exhibits limited expression in normal tissues but shows ectopic overexpression across multiple cancer types including lung, breast, and glioma 234. In lung adenocarcinoma, ITPKA overexpression is transcriptionally activated by TFAP2A and regulated by epigenetic gene body methylation, with methylation appearing early during malignant transformation 23. ITPKA promotes tumorigenesis through distinct mechanisms: its actin bundling activity primarily drives cancer cell migration and invasion 5, while its InsP3-kinase activity enhances these effects under specific conditions 5. In glioma, ITPKA phosphorylates PYCR1 at serine 29, stabilizing the protein and promoting oncogenic function 4. Notably, ITPKA exhibits context-dependent roles—it functions as an oncogene in most cancers but acts as a tumor suppressor in ovarian cancer through P53 stabilization and senescence induction 6. Physiologically, ITPKA participates in nociception, sensorimotor gating, and energy metabolism 7. ITPKA emerges as a potential therapeutic target and early diagnostic biomarker across multiple malignancies 8.