Recently, based on the accumulated evidence of the strong induction of adaptive IRE1α in MM patients and our findings showing the inhibitory effect of another second-generation BCR-ABL TKI, nilotinib, on IRE1α in pancreatic β cells [3], we first demonstrated the anti-myeloma effects of nilotinib, which were possibly facilitated by inhibiting adaptive IRE1α and reciprocally inducing pro-apoptotic CHOP via the PERK pathway [10]. This evidence concerns the gene DDIT3 and plasma cell myeloma.