The proprotein convertase subtilisin kexin type 9 (PCSK9), identified in 2001 with its gene characterization in 2003 [8], acts as a negative regulator of LDLR by binding to LDLR and therefore increases LDL-C [9], leading to atherosclerotic coronary artery disease [4], with or without endothelial dysfunction [10]. Here, LDLR is linked to endothelial dysfunction.