The mechanism of TKI resistance is subdivided into ABL1 mutation-dependent (acquired resistance) which means loss of response, and ABL1 mutation-independent (primary resistance), which results in conformational changes of the TKI binding site due to mutation in SH1 of ABL1.33 Therefore, a new target therapy or combining TKI is required to cure CML. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.