Though imatinib significantly improves outcomes in patients with BCR–ABL1‐driven CML, resistance emerges unavoidably after long‐term treatment, such as M244, G250, Q252, Y253, and E255 located in the P loop, T315 and F317 in the ATP‐binding region, M351 and F359 in SH2 contact and C‐lobe region, and H396 in the activation loop.40 The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.