Majority of clinically diagnosed FH patients carry autosomal dominant loss-of-function (LOF) mutations in the low-density lipoprotein receptor (LDLR) and apolipoprotein-B (APOB) genes or gain-of-function (GOF) mutations in the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene (Alallaf et al., 2017; Awan et al., 2019; Al-Waili et al., 2020). Here, LDLR is linked to familial hyperaldosteronism.