This was firstly suggested by the inability of GSK-J4, which inhibits the demethylase activity of KDM6A, to reduce the sensitivity of CML cells to imatinib, and was further substantiated by the observation that an enzyme-dead KDM6A mutant, similar to wild-type KDM6A, recovered the resistance to imatinib in CML cells with endogenous KDM6A knocked out. This evidence concerns the gene MBD2 and chronic myelogenous leukemia, BCR-ABL1 positive.