In the bleomycin-induced pulmonary fibrosis mouse model, RGS2−/− mice had significantly increased pulmonary deposition of collagen compared to RGS2+/+ mice, and this collagen is predominately produced by differentiated pulmonary fibroblast cells, suggesting that endogenous RGS2 in pulmonary fibroblast cells should function as an anti-fibrotic gene. This evidence concerns the gene RGS2 and pulmonary fibrosis.