In both models, depletion of ILC2s significantly diminished fibrosis development in the Hps1−/− mice, suggesting that ILC2-mediated mechanisms contributed to optimal CHI3L1-induced amplified fibrotic responses in the bleomycin-induced pulmonary fibrosis in Hps1−/− mice. The gene discussed is CHI3L1; the disease is pulmonary fibrosis.