These factors may be compounded by genetic abnormalities that dysregulate key lipid metabolic pathways and cause steatosis, for example, overexpression of genes involved in hepatic lipid synthesis (sterol regulatory element binding protein (SREBP), fatty acid synthase (FAS), stearoyl-coenzyme A (CoA) desaturase (SCD), etc.)and hepatic lipid uptake (low-density lipoprotein receptor, cluster of differentiation 36 (CD36)), or downregulation of genes required for hepatic lipid metabolism and transportation (apolipoprotein B), which is the toxic accumulation of lipids within hepatocytes.3 4. This evidence concerns the gene FASN and steatosis.