Of note, the levels of IL-1β in COVID-19 patients were comparable to those seen in monogenic autoinflammatory disorders of IL-1β excess, whereas the levels of IL-18 were lower in COVID-19 patients relative to the levels observed in autoinflammatory IL-18opathies that predispose to MAS (Supplemental Figure 7B). This evidence concerns the gene IL1B and macrophage activation syndrome.