We have recently used a mouse model in which the AMPK phosphorylation site Ser871 on HMGCR was mutated to Ala (Hmgcr KI mice) and demonstrated that this phosphorylation event inhibits cholesterol synthesis in vivo and is important for suppressing the development of hepatic steatosis in response to high carbohydrate feeding [29]. The gene discussed is HMGCR; the disease is fatty liver disease.