The possible mechanisms of pro-lung cancer effects could be explained by the findings that IL-33 can promote EMT by increasing the expression of CD146 in airway epithelial cells, induce ILC2 to produce IL-13, and polarize M2 macrophages to generate IL-13 and TGF-β (64), these factors can promote pulmonary fibrosis, which might induce lung cancer. Here, TGFB1 is linked to pulmonary fibrosis.