Overexpression of T-cadherin in endothelial cells attenuated insulin-induced PI3K/Akt/mTOR pathway activation and simultaneously reduced insulin-stimulated eNOS activation, migration, and angiogenesis, suggesting the role of endothelial dysfunction induced by T-cadherin in atherosclerosis (Philippova et al., 2012). The gene discussed is AKT1; the disease is endothelial dysfunction.