Pathophysiologically, FH is caused by genomic variants of key genes that are involved in the metabolism of cholesterol, including the low-density lipoprotein receptor (LDLR), the proprotein convertase subtilisin/kexin type 9 (PCSK9), and the apolipoprotein B (APOB) genes (Henderson et al., 2016; Sharifi et al., 2017; Vrablik et al., 2020). The gene discussed is APOB; the disease is familial hyperaldosteronism.