Moreover, the IL-33/ST2 axis plays an important role in pulmonary fibrosis, as shown in two experimental models in which mice treated with a profibrotic substance exhibited a linear increase in IL-33 expression, an aspect explained by the alleged activation of fibroblasts by inflammatory cytokines triggered by the interaction between IL-33 and ST2L [179,180]. This evidence concerns the gene IL33 and pulmonary fibrosis.