We hypothesize that these effects could be a part of a secondary survival cellular mechanism to counteract the activation of the endothelial reticulum and cell death pathways since Akt inhibition promotes autophagy (Degtyarev et al., 2008) and activation of JNK reduces autophagy and increases apoptosis providing a promising strategy for prostate cancer therapy (Zhu et al., 2017). This evidence concerns the gene AKT1 and prostate cancer.