LDLR and familial hyperaldosteronism: Although the clinical features of both heterozygous and homozygous mutations in monogenic FH have significantly been described, very few is known about “double-heterozygous” or digenic FH phenotypes, where we have a combination of mutations between any two of the known FH-causing genes including APOB, LDLR, PCSK9, and LDLRAP1 (Tada et al., 2011; Cuchel et al., 2014).