This study further allowed the conclusion that the different branches of the UPR signaling are not redundant, and, therefore, Sunitinib-mediated overexpression of NF-kB and RCC survival were mediated by IRE1α signaling, while the Sunitinib-mediated pro-tumorigenic cytokine increase was dependent of the PERK signaling [47]. This evidence concerns the gene EIF2AK3 and renal cell carcinoma.