In our study, we observed that COVID-19 patient-serum-treated human endothelial cells show features of endothelial dysfunction, including increased monocyte adhesion to activated endothelium, concurrent with decreased expression of vasoprotective molecule KLF2 and eNOS, and increased expression of ICAM1, and VCAM1; these observations raise the possibility that KLF2 serves as a new and promising target for therapeutic intervention of endothelial dysfunction accompanying COVID-19 (Supplementary Fig. 5). The gene discussed is KLF2; the disease is COVID-19.