The complexity underlined by the previous observations indicating that i) anti-ApoA-1 IgG are associated with a more favorable lipid profile in FH children but lower miR-33a levels and ii) that these antibodies could increase both pro-atherogenic (HMGCR increase) and anti-atherogenic pathways (SREBP-2, LDLR) in vitro prompted us to evaluate the global result of exposing human macrophages to anti-ApoA-1 IgG in terms of foam cell formation. The gene discussed is LDLR; the disease is familial hyperaldosteronism.