The best‐known human genetic dyslipidemia is familial hypercholesterolemia (FH), in which elevated LDL cholesterol and apo B result not from overproduction but rather defective catabolism due to loss‐of‐function variants in the LDLR gene encoding the LDL receptor, or less frequently in the APOB, PCSK9 and LDLRAP1 genes encoding apo B or proprotein convertase subtilisin kexin type 9 (PCSK9) and LDL receptor adaptor protein 1 (LDLRAP1), respectively [3]. This evidence concerns the gene APOB and familial hyperaldosteronism.