Despite the evidence that IL-1β and IL-18 are key contributors to the development of cytokine storm syndromes, there has been little research on which inflammasomes are activated in the majority of hyperinflammatory diseases, though recent data has been obtained in severe COVID-19 [45], with studies demonstrating activation of the NLRP3 inflammasome in monocytes and macrophages in SARS-CoV-2-infected patients [48, 49]. The gene discussed is IL1B; the disease is COVID-19.