CCL2 and COVID-19: Experimental work demonstrated that ACE2 deficiency resulted in up-regulation of Angiotensin II-induced expression of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, tumor necrosis factor -α, monocyte chemoattractant protein-1 and TGF-β that may contribute to the cytokine storm in humans; a major driver of illness severity during SARS-COV2 infection.43,44 However, an overly activated RAS may represent a part of complex multistep mechanism mediating abnormal inflammatory and thrombotic processes in COVID-19 to be further investigated.