RETSAT and metabolic syndrome: 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.