AKT1 and aortic valve insufficiency: However, aortic-regurgitation does not produce pure volume-overload (Wilson and Lucchesi, 2014), and others have reported that activation of Akt/mTORC1 pathway has a central role in promoting eccentric hypertrophy in aorto-caval shunts with the level of pathway activation being a function of LV end-diastolic stress (Ikeda et al., 2015) (Figure 4).