Moreover, prolonged ischemia in I/R-AKI is often associated with a decrease of autophagic flux rather than an increase for the following reasons: the consumption and depletion of essential autophagic components after long starvation periods, the reactivation of mTOR activity and the inhibition of master regulators of autophagy such as ATG3, AMBRA1 and Beclin1 by caspases, which are activated in response to prolonged stress (Pallet, 2014). This evidence concerns the gene BECN1 and acute kidney injury.