Previous studies have shown that KLF2 is a negative regulator of endothelial activation, dysfunction, and thrombosis.37–39 KLF2 expression was downregulated by treatment with various inflammatory cytokines, such as TNF-α40 and IL-1β,20 two of which are frequently observed cytokine storm in COVID-19 patients.10 A recent study from Fang laboratory demonstrated reduced endothelial KLF2 expression in lung autopsies of COVID-19 patients, compared with control subjects. This evidence concerns the gene IL1B and COVID-19.