Therefore, based on our data and published literature,41 it is plausible that KLF2 suppresses COVID-19-induced endothelial dysfunction by multiple mechanisms, which may involve: (1) enhancing endothelial quiescence and pulmonary vascular integrity; (2) boosting eNOS dependent NO production; (3) inhibiting ICAM-1, VCAM-1, and E-selectin mediated monocyte adhesion via reported suppressing NF-kB signaling pathway; (4) hemostatic and anti-thrombotic function mediated by thrombomodulin upregulation and PAI-1 downregulation. This evidence concerns the gene KLF2 and COVID-19.