We have previously established that young Pcyt2 + /- mice (2-mo) show early changes in gene expression that contributed to the adult development of NASH, including dysregulation of genes and pathways involved in fatty acid oxidation, triglyceride and ammonia metabolism, hepatic steatosis and abnormal liver physiology [15,16]. This evidence concerns the gene PCYT2 and metabolic dysfunction-associated steatohepatitis.