Consistent with its role in inflammation and disease in mouse models, our data suggest that SARS-CoV-2-induced RIPK1 activation may also contribute to COVID-19-associated CRS, which is supported by evidence that nsp12, a viral RNA polymerase for SARS-CoV-2 replication, binds RIPK1 in the COVID-19 interactome [55]. The gene discussed is RIPK1; the disease is COVID-19.