Genetic ablation of ST2, administration of anti-IL-33, or lentiviral overexpression of the sST2 decoy receptor during the inflammatory phase of the BLM model attenuated IL-13, IL-33, and TGF-β expression while halting pulmonary fibrosis and improving survival rates in BLM-treated mice [64, 73]. This evidence concerns the gene IL33 and Bloom syndrome.