Since LDLR is a gene-encoding receptor responsible for cholesterol intake, SOAT1 is for esterification, and SQLE is for cholesterol biosynthesis [37], a conclusion was drawn as the following: prostate cancers that progress to lethal disease rely on de novo cholesterol synthesis via SQLE, rather than transcellular uptake via LDLR or cholesterol esterification via SOAT1 [104]. The gene discussed is SOAT1; the disease is Familial prostate cancer.