When balanced with metabolically favorable aspects of activated ChREBP, e.g. de novo lipogenesis in adipose tissue24, and fatty acid desaturation49 and suppression of SREBP2-mediated detrimental cholesterol overload50 in liver, pharmacological inhibition of RetSat and lower ChREBP activity in liver may have therapeutic potential to treat hepatic steatosis, dyslipidemia and hyperglycemia. The gene discussed is SREBF2; the disease is Hepatic steatosis.