These include the coagulation factor XIIIA (F13A1) that is elevated in COVID-19 patients and is higher in nonsurvivors [57], complement C1QA and C1QB that are associated with complement activation and endothelial dysfunction in COVID-19 (56), as well as proinflammatory cytokines and chemokines such as CXCL8, CCL2, CXCL2, and MMP9 which impairs epithelial tight junction integrity and barrier functions [70]. This evidence concerns the gene CCL2 and endothelial dysfunction.