To discern the potential role of T-cadherin in the development of fibrosis or endothelial dysfunction, we enrolled two animal models involving wild-type (WT) and T-cadherin knockout (Cdh13−/−) mice: a bleomycin-induced model of lung injury and an angiotensin II-induced model of endothelial dysfunction. The gene discussed is CDH13; the disease is endothelial dysfunction.