Given that IL-33 is critical for the function of CD8+ T cells in the antiviral response to persistent SARS-CoV2 infection and may contribute to viral elimination and that IL-33-induced hyperinflammation conversely exacerbates COVID-19-related complications, a better understanding of the exact role of IL-33 and how the IL-33/ST2 axis is manipulated is of vital importance to the development of effective strategies for the prevention and treatment of COVID-19. This evidence concerns the gene CD8A and COVID-19.