PCSK9 and familial hyperaldosteronism: As regards the inflammatory profile, previous studies showed that PCSK9-i did not reduce hs-CRP levels in the general population [41] and the same finding was observed in our FH cohort; however, Kuhnast et al. showed that these drugs could suppress the inflammatory state by reducing monocyte recruitment and subsequently the necrotic core macrophages in an atherogenic mouse model [42].