KLF2 and COVID-19: Specifically, we addressed: (1) COVID-19 patient serum downregulated KLF2 expression in human endothelial cells; (2) High level of TNFα and IL-1β in COVID-19 patient serum could partially explain the mechanism of KLF2 downregulation; (3) KLF2 downregulation-induced monocyte adhesion could explain endothelialitis and lympho-monocytic cells infiltration in COVID-19 patients; (4) genetic and pharmacological activation of KLF2 by KLF2 adenovirus, atorvastatin, and tannic acid ameliorates patient-serum-induced monocyte adhesion.