Our findings support combining FLT3 inhibitors with BCR::ABL1 TKIs or single treatment of ponatinib for the treatment of FLT3+ CML patients, which abolishes FLT3-TAZ signaling, restores TKI sensitivity, and enhances therapeutic efficacy. This evidence concerns the gene FLT3 and chronic myelogenous leukemia, BCR-ABL1 positive.