Interestingly, in a mouse model of nonalcoholic steatohepatitis (NASH), pharmacological inhibition of ATP-citrate lyase reduced hepatic steatosis, fibrosis, inflammation, blood glucose, and triglycerides [112], suggesting that the beneficial effect of BT2 may also be ascribed to this ATP-citrate lyase inhibition rather than to BCKD activation. The gene discussed is ACLY; the disease is metabolic dysfunction-associated steatohepatitis.