The lack of phosphorylated MLKL and the fact that genetic deletion of MLKL did not alter disease parameters in our SARS-CoV-2 mouse models mimicking mild and severe COVID-19 indicates that, while necroptosis is primed upon SARS-CoV-2 infection, MLKL dependent membrane disruption, cytokine release and death do not contribute to disease. This evidence concerns the gene MLKL and COVID-19.