AKT1 and endothelial dysfunction: The underlying cellular and molecular mechanisms appear to involve activities of hepatic stellate cells (HSCs), endothelial dysfunction, the factor Xa or thrombin, transforming growth factor-beta (TGF-β)/SMAD signaling, extracellular signal-regulated kinase (ERK) signaling, signal transduction from AKT to c-RAF, AKT signaling, and the nitric oxide (NO) pathway [13, 16–20].