Previous work showed that mTORC1 inhibition by rapamycin can promote Akt-mediated death in tumor cells subjected to oxidative therapies.13 Given that the regulation of Akt activity by eIF2αP depends on mTORC1 (Figure 5), we were interested to examine the effects of rapamycin on the sensitivity of eIF2αP-proficient and -deficient cells to oxidative stress. Here, AKT1 is linked to neoplasm.