ETNK1 (ethanolamine kinase 1) catalyzes the phosphorylation of ethanolamine, a rate-controlling step in phosphatidylethanolamine (PE) biosynthesis via the CDP-ethanolamine pathway 1. This lipid metabolic enzyme functions in the cytoplasm and at cellular membranes to regulate phospholipid composition. Mechanistically, ETNK1 controls PE synthesis, which localizes to the outer plasma membrane and coordinates post-transcriptional regulation of membrane proteins. In T follicular helper cells, ETNK1-dependent PE synthesis prevents internalization and degradation of CXCR5, promoting humoral immunity 1. ETNK1 also contributes to ferroptosis resistance by regulating cellular phospholipid profiles; hypoxia-induced suppression of ETNK1 expression reduces ferroptosis sensitivity in cancer cells 2. Clinically, ETNK1 mutations are implicated in myeloid neoplasms. While historically associated with atypical chr12 myeloid leukemia (aCML) diagnosis 34, ETNK1 mutations occur across diverse myeloid malignancies including myelodysplastic syndrome (46%), MDS/MPN overlap (21%), acute myeloid leukemia (18%), and myeloproliferative neoplasm (15%) 5. ETNK1 mutations typically represent early, dominant clonal events accompanied by concurrent mutations (ASXL1, TET2, EZH2), and may promote genomic instability 5. ETNK1 is recommended for inclusion in myeloid gene panels 6, and represents a potential therapeutic target for myeloid neoplasms 7.