Moreover, it has demonstrated that the novel AT2R agonist, β-Pro7 Ang III, was able to attenuate lung fibrosis through its ability to ameliorate the pro-fibrotic impact of TGF-β1 on myofibroblast accumulation and ECM deposition, while being able to promote collagen-degrading MMP-2 activity after as little as seven days of treatment. The gene discussed is TGFB1; the disease is pulmonary fibrosis.