Many of these immune pathways (“IL-1 signaling”, “IL-4/13 signaling”, “Neutrophil degranulation”, and “Immunoregulatory interactions”) were also enriched by persistent genes in the two validation datasets of COVID-19 and sepsis patients (Figure S4), as well as in persistent genes of non-survivors even after splitting into COVID-19 and non-COVID-19 sepsis patients (Figure S2D), suggesting shared mechanisms of mortality between these two diseases. This evidence concerns the gene IL4 and Sepsis.