An intronic variant in NOS3 is also prioritized as a core causal variant of CAD alongside CCM2 both being important to blood vessel morphology and function (20) with several other rare and common variants in GUCY1A3 PDE5A and PEDE3A (16, 20, 36, 83, 84) highlighting the importance of the NO/cGMP signaling pathway to atherosclerosis and CAD risk. This evidence concerns the gene PDE5A and coronary artery disorder.