To further explore a possible causal link between the presence of anti-ApoA-1 antibodies, lower miR-33a levels, and a more favorable lipid profile in FH children, we first tested the ability of polyclonal anti-ApoA-1 IgG or control IgG to modulate the in vitro miR-33a production in human monocyte-derived macrophages (HMDM). Here, APOA1 is linked to familial hyperaldosteronism.