Several pro-inflammatory cytokines have been described in COVID-19 patients and are associated with the disease’s immunopathogenesis. Among them, IL-1β and TNF-α stand out for playing a central role in this context (26, 156). The respiratory failure characteristic of SARS-CoV-2 infection, especially in individuals who develop the most severe forms of the disease, occurs independently of infection or viral replication in the epithelial bronchial cells and probably occurs due to exacerbated inflammatory dysregulation, resulting from activation of the NLRP3 inflammasome pathway and consequent release of IL-1β (158). However, although several articles have shown an increase in IL-1β production in COVID-19 patients and early treatment with IL-1 receptor blockers has helped prevent respiratory failure (159), its exact role in the immunopathogenesis of the disease has not yet been fully described.