The wild type PNPLA3 has function of triglyceride hydrolase and acetylCoA-independent transacylase activity, and loss of its function consequently leads to an accumulation of triglycerides droplets and retinyl esters within hepatocytes and cause endoplasmic reticulm (ER) stress and damage to liver cells eventually leading to fatty liver.12 Studies have shown that loss of function of PNPLA3 leads to increased hepatic steatosis and elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. This evidence concerns the gene GPT and fatty liver disease.