IL-33 may contribute to the pathogenesis of severe COVID-19 through dampening antiviral responses and through contributing to lung fibrosis, neutrophil migration, thromboses, and mast cell and eosinophil activation, all of which has been reviewed by Murdaca et al. (2022) and Zizzo and Cohen (2020) [50,116]. This evidence concerns the gene IL33 and COVID-19.