Variants in ABCG5 and ABCG8 can cause sitosterolemia, a rare disease characterized by increased circulating levels of plant sterols,14 and variants in LIPA can induce a disease characterized by cholesterol ester storage due to lysosomal acid lipase deficiency.15 Finally, rare variants in APOE have also been associated with FH-like phenotypes.13 Of interest, the STAP1 gene recently suffered a downgrade as a possible cause of the FH phenotype since no cosegregation of high LDL-C was encountered in individuals bearing genetic variants within the same family or in experimental animals.16,17. This evidence concerns the gene STAP1 and familial hyperaldosteronism.