In fact, as previously mentioned, critical COVID-19 assumes the connotations of a hyperferritinemic syndrome or an autoinflammatory febrile disease, in which an aberrant activation of the NLRP3 inflammasome, in this case resulting from the conspicuous presence of monocytes-macrophages and viral products (e.g., viroporins), provokes intense production of IL-1α and IL-1β, which ultimately drive hyperinflammation and severe ARDS (7, 27), whereas IL-6 would now play regulatory roles. This evidence concerns the gene IL6 and COVID-19.