We found that p-AKT was decreased while PTEN, a negative regulator of p-AKT, was increased in cells treated with TGN, LPS or IL-6 (Figures 2I, J; Supplementary Figures 1 A, B), suggesting that the damage to EC function resulting from sepsis was likely mediated by the AKT pathway. The gene discussed is AKT1; the disease is Sepsis.