Resistance to imatinib in CML was also shown to result from the activation of ATF6α, which appears mediated by the protein disulfide isomerase 5 (PDIA5) upon ER stress and a PDIA5 inhibitor, 16F16, increased cells’ sensitivity to treatment with imatinib [163]. The gene discussed is PDIA5; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.