CDIPT (CDP-diacylglycerol--inositol 3-phosphatidyltransferase) catalyzes the biosynthesis of phosphatidylinositol (PtdIns), the foundational lipid for all phosphoinositide species 1. The enzyme is localized to the endoplasmic reticulum and participates in autophagosome formation by being enriched in ER subdomains involved in phospholipid synthesis 2. Loss of CDIPT function results in severe cellular pathology, as demonstrated in zebrafish mutants that develop intestinal mucosal injury characterized by ER-Golgi disruption, mitochondrial depletion, and chr16 ER stress-mediated inflammation 3. While CDIPT deficiency does not prevent early myogenesis, it impairs triad formation in skeletal muscle, resulting in smaller T-tubule areas and decreased motor performance 1. The gene shows clinical significance in multiple disease contexts: CDIPT mutations are associated with resistance to AKT inhibitor therapy in cancer patients 4, and the gene is identified as a target of miR-20a-5p in psoriasis-obesity comorbidity 5. Additionally, CDIPT expression is upregulated in oral premalignant lesions and squamous cell carcinomas of smokeless tobacco users 6, suggesting roles in both metabolic disorders and carcinogenesis through dysregulated phosphoinositide signaling pathways.