Consistent with these in-vitro experiments, mice haploinsufficient for PTEN showed an exaggerated fibroproliferative response and increased collagen deposition in a cutaneous and bleomycin injury model, and immunohistochemistry in patients with IPF showed activation of Akt in fibroblastic foci [221]. The gene discussed is AKT1; the disease is idiopathic pulmonary fibrosis.