Furthermore, ICG-001’s specific inhibition of CBP/β-catenin signaling promoted differentiation and sensitized quiescent, drug-resistant chronic myelogenous leukemia (CML) cells to Bcr-Abl tyrosine kinase inhibitors, such as imatinib [44]. Here, CREBBP is linked to chronic myelogenous leukemia, BCR-ABL1 positive.