In our experiments, we were able to demonstrate that the main actors involved in the ferroptotic process, namely, GPX4, SLC7A11, FTH1, and SAT1, were all regulated by serum from COVID-19 non-survivors and, in the opposite direction, by TNFR1 silencing, strongly suggesting that TNFα is functionally involved in the association between COVID-19 and ferroptosis in endothelial cells. The gene discussed is TNF; the disease is COVID-19.