Phosphatase restoration by these compounds contributes to enhanced TKI response (as in the case of OP449), as well as allowing the overpass of resistance even in those cells carrying a drug-resistance mutation in the BCR-ABL1 kinase domain, as has been shown in primary CD34+ CML cells or in a mouse models implanted with drug-resistant Ba/F3-p210T315I Bcr-Abl1 [142]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.