TP53 and chronic myelogenous leukemia, BCR-ABL1 positive: In CML cells with Bcr–Abl-independent imatinib resistance, the resistance mechanism includes the aberrant acetylation of p53 and other proteins due to the upregulation of HDACs and the downregulation of HATs, indicating HDACs as targets for imatinib-resistant leukemia cells (135).