In these patients, the LDL-C-lowering effect is greater in those with partially functioning LDLR compared to those with negative or null–-null LDLR mutations, suggesting that for PCSK9 inhibitors to be effective in FH, at least one non-null allele coding a partially functioning LDLR must be present [45,49,50,51]. This evidence concerns the gene LDLR and familial hyperaldosteronism.