Several studies have demonstrated that adaptive UPR activation mediated by common oncogenic alterations in leukemia can increase the ability of cells to cope with ER stress and restore ER homeostasis, including BCR-ABL [42], PML-RARα [43], and enhanced MYC, N-Ras, and c-Jun activity [41, 44, 45]. The gene discussed is NRAS; the disease is leukemia.