During neonatal influenza (H3N2) virus infection, lung accumulation of IL-17A-producing γδ T cells, associated with the increase in lung epithelial cell-derived IL-33, resulted in IL-17A-dependent IL-33-mediated promotion of local type II immunity and infiltration of group 2 innate lymphoid cells and regulatory T cells to the lung, which thereby led to the augmented amphiregulin secretion and tissue repair [14]. The gene discussed is IL33; the disease is influenza.