Given that IPF is not driven by antigen-specific mechanisms and that endogenous factors play a significant role in its pathogenesis, there is a possibility that ILC2s, which are activated by endogenous factors and produce tissue repair factors such as IL-4, IL-13, and amphiregulin1, could have a more direct involvement in fibrosis, as compared to adaptive immune cells. This evidence concerns the gene IL13 and idiopathic interstitial pneumonia.