In contrast, when Hps1−/− mice were bred with Rag1−/− mice to deplete T cells, Hps1−/−Rag1−/− double-mutant mice were not protected from bleomycin-induced lung fibrosis development (Figure 4E), suggesting Th2s did not contribute to fibrosis development in this model. The gene discussed is RAG1; the disease is pulmonary fibrosis.