Dietary cholesterol and fat is well known to elicit an accumulation of cholesterol esters and triglycerides in the liver possibly via an enhancement of cholesterol-7α hydroxylase activity for bile acid synthesis, and a suppression of HMG-CoA reductase activity for rate-limiting cholesterol synthesis, contributing to hyperlipidemia [19]. The gene discussed is HMGCR; the disease is hyperlipidemia.