Lipid metabolism changes in FH patients, including reduced low-density lipoprotein receptor (LDLR)-mediated low-density lipoprotein cholesterol (LDL-C) catabolism, impaired apolipoprotein B (APOB)-mediated LDL clearance, and increased proprotein convertase subtilisin/kexin type 9 (PCSK9) levels, mediate post-translational destruction of LDLRs (Chiou and Charng, 2016, Sturm et al., 2018). This evidence concerns the gene APOB and familial hyperaldosteronism.