Our findings clearly showed that the favorable effect of PCSK9-i treatment on lipoprotein functions could contribute to the CV benefit of these drugs beyond LDL-c reduction in subjects at high CV risk such as FH in clinical practice; however, a designed study with a wider cohort of subjects is needed to assess the effect of PCSK9-i therapy on these pathways in FH subjects. The gene discussed is PCSK9; the disease is familial hyperaldosteronism.