IL-33, a crucial inflammatory cytokine, can not only enhance the accumulation of neutrophil extracellular traps, promote the transformation of macrophages to the M2 type, inhibit the function of plasmacytoid dendritic cells to produce type I interferon, and drive type 2 innate lymphocytes (ILC2) differentiation, but it can also promote the proliferation of Th17 cells and limit the function of CD4+/CD8+ cells during the pathogenesis and development of COVID-19. The gene discussed is CD4; the disease is COVID-19.