It is hypothesized that inflammasomes are crucial in driving the pathology associated with severe COVID-19, since inflammasome activation leads to maturation of IL-1β and IL-18, along with the formation of pores in the cell membrane leading to the release of tissue factor (TF) positive microvesicles and netosis in neutrophils, both of which contribute to coagulation in the vasculature (as reviewed [45]). The gene discussed is IL1B; the disease is COVID-19.