PEMT (phosphatidylethanolamine N-methyltransferase) is an endoplasmic reticulum-localized enzyme that catalyzes the sequential three-step methylation of phosphatidylethanolamine to phosphatidylcholine (PC), serving as an alternative pathway for PC biosynthesis independent of the Kennedy pathway 1. The gene generates three distinct transcripts through differential promoter usage, with the highest expression in liver, followed by heart and testis, enabling tissue-specific regulation 2. PEMT activity is regulated by substrate availability (phosphatidylethanolamine and S-adenosylmethionine) and estrogen, with estrogen-responsive elements in the gene promoter explaining why premenopausal women show greater resistance to choline deficiency 3. Clinically, PEMT dysfunction is associated with nonalcoholic fatty liver disease (NAFLD), as the V175M polymorphism represents a loss-of-function mutation occurring in 67.9% of NAFLD patients versus 40.7% of controls 4. Additionally, visceral adipose tissue PEMT expression correlates with type 2 diabetes and non-alcoholic steatohepatitis (NASH) progression, and the rs4646404 variant associates with altered fat distribution and diabetes-related traits 5. These findings position PEMT as a key regulator of lipid metabolism with implications for metabolic disease susceptibility.