Critically ill COVID-19 patients are characterized by a severely dysregulated cytokine profile and elevated neutrophil counts, which are thought to contribute to disease severity . However, to date it remains unclear how neutrophils contribute to pathophysiology during COVID-19 . Here, we assessed the impact of the dysregulated cytokine profile on the tightly regulated cell death program of neutrophils . We show that in a subpopulation of neutrophils, canonical apoptosis was skewed towards rapidly occurring necroptosis . This phenotype was characterized by abrogated caspase-8 activity and increased RIPK1 levels, favoring execution of necroptosis via the RIPK1-RIPK3-MLKL axis, as further confirmed in COVID-19 biopsies . Moreover, reduction of sFas-L levels in COVID-19 patients and hence decreased signaling to Fas directly increased RIPK1 levels and correlated with disease severity . Our results suggest an important role for Fas signaling in the regulation of cell death program ambiguity via the ripoptosome in neutrophils during COVID-19 and a potential therapeutic target to curb inflammation and thus influence disease severity and outcome.