Deleterious mutations in LDLR are the most common cause of FH [8,45,46]; loss of function variants in LDLRAP1 have been documented to cause high LDL-cholesterol levels with a recessive form of inheritance (38); variants in APOB have been known to cause both low and high LDL-cholesterol levels [16,47–49]; and loss of function variants that cause low LDL-cholesterol have been identified in PCSK9 [50–52]. Here, APOB is linked to familial hyperaldosteronism.