LDLR and familial hyperaldosteronism: Hence, in attention to critical and well-established role of LDLR, APOB, and PCSK9 genes in LDL-C hemostasis and metabolism, therapeutic manipulation of related miRs, via miR mimics or inhibitors, can be an efficient and attractive approach for lowering elevated LDL-C and reducing risk of CV events in FH patients (Fig. 1).