Besides, the phenotypic severity exists on a continuum with a considerable overlap between heterozygous and homozygous FH (including double heterozygotes, compound heterozygotes and true homozygotes), though generally the mean LDL-C level increased as follows: LDLR-negative homozygotes > compound LDLR heterozygotes > LDLR-defective or LDLRAP1 homozygotes > APOB or PCSK9 homozygotes > double heterozygotes > heterozygous FH [17]. This evidence concerns the gene APOB and familial hyperaldosteronism.