Activationof protein kinase B (PKB), mitogen-activated protein kinase (p42/44MAPK),Ca2+ calmodulin-dependent protein kinase, and adenosine monophosphate (AMP)-activated protein kinase(AMPK) collectively promote the release of vasodilator factors and the productionof endothelial NO, thereby further inhibiting platelet activation,atherosclerosis, and thromboinflammatory responses [32, 33, 34, 35, 36].Additionally, HDL-C enhances prostacyclin (PGI2) synthesis and acts inconjunction with NO to inhibit platelet activation, thus reducing thrombotic riskand the incidence of CVD [37, 38, 39, 40, 41]. Here, WNK2 is linked to atherosclerosis.