APOB and familial hyperaldosteronism: LDLR plays an important role in cholesterol homeostasis, and this is well illustrated by the fact that more than 2000 LDLR variants have been found in patients with familial hypercholesterolemia (FH) that can impair LDLR activity at different levels and therefore are classified according to their phenotypic behavior as follows: class 1 (no protein synthesis), class 2 (partial or complete retention of LDLR in the endoplasmic reticulum, class 3 (defective binding to apoB, class 4 (defective endocytosis) and class 5 (diminished LDLR recycling capacity) [5].