In cancer, the overexpression of sCLU mediates in part the activation of the PI3K/Akt pathway and increased the per se phosphorylation of Akt, with the consequent Akt-induced phosphorylation of Bad, thus, inhibiting TNFα-induced apoptosis [48]; otherwise, in prostate cancer, proapoptotic nCLU decreased, while antiapoptotic sCLU increased [49, 50]. Here, AKT1 is linked to cancer.