Familial hypercholesterolemia (FH) is a genetic cause of premature myocardial infarction (PMI) due to lifelong elevated serum low‐density lipoprotein cholesterol (LDL‐C) levels.1 As an autosomal genetic disease, low‐density lipoprotein receptor (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin‐kexin type 9 (PCSK9) and low‐density lipoprotein receptor adaptor protein 1 (LDLRAP1) genes are the most important pathogenic genes of FH.2, 3 Mutations of LDLR, PCSK9 and APOB genes are autosomal dominant inheritance. The gene discussed is LDLR; the disease is familial hyperaldosteronism.