WNK2 and endothelial dysfunction: They dysregulated the renin-angiotensin-aldosterone system and the role of ACE2, causing oxidative stress damage, endothelial dysfunction, and the activation of the von Willebrand factor, and dysregulated the immune response, role of the complement system, neutrophil extracellular traps (NETs), and mitogen-activated protein kinases (MAPKs) pathways.