Although some have shown that prostate cancer cells can respond adaptively via eIF2α phosphorylation to reset global protein synthesis and promote aggressive tumor development [19], in other reports it appears that ER stress can lead a cell to either undergo apoptosis via upregulation of Fas cell surface death receptor (Fas) or to adapt via phosphorylation of eIF2α and upregulation of activating transcription factor 4 (ATF4), mechanisms that lead to sustained ER stress and result in cancer cell death via caspase-3 and others [20]. This evidence concerns the gene ATF4 and prostate carcinoma.