The inability to kill infected or activated antigen-presenting cells in patients with either MAS or COVID-19 could result in persistent interactions between T cells and antigen presenting cells, culminating in hyperproduction of cytokines as a result of overstimulation of both cell types.1 However, by contrast with COVID-19, IFNγ is not impaired in MAS, and is a major driver of disease. In MAS, IFNγ-producing CD8+ T-cell populations are elevated in primary and secondary lymphoid organs, leading to IFNγ-driven macrophage hyperactivation and haemophagocytosis.1, 3