Despite this apparent functional redundancy, lipin1 is emerging as a key player in ethanol-induced steatosis [38] and a single nucleotide polymorphism in LPIN1 is associated with the severity of liver damage and fibrosis progression in pediatric human patients with histological non-alcoholic fatty liver disease (NAFLD) [39], suggesting that liver lipin1 dysfunction may contribute to steatosis-related liver pathogenesis. This evidence concerns the gene LPIN1 and steatosis.