Collectively, MAKV-8 appears to be an attractive drug candidate for further consideration in CML therapies, especially considering that the inhibition of HDAC1 and HDAC2, upregulated in LSCs versus HSCs from patients, strongly impacts the transcription of proteins essential for tumor cell survival [21]. This evidence concerns the gene HDAC2 and chronic myelogenous leukemia, BCR-ABL1 positive.