CD36 and familial hyperaldosteronism: Interaction between CD36 and oxLDL-C promote a pro-inflammatory and pro-atherogenic response [31] and the increased expression of pro-atherogenic and pro-inflammatory genes in FH monocytes, particularly observed in monocytes derived from FH subjects with ATX, as well as their correlation with plasma oxLDL-C and IMT demonstrated herein, supports the important contribution of oxLDL-C in the progression of atherosclerosis.