These efforts have led to the development of highly effective specific inhibitors in other types of leukemia by targeting the oncoproteins causing APL (PML/RAR; ATRA) and CML (BCR/ABL; imatinib), but have failed to effectively target others in AML, such as the FLT3-ITD growth factor receptor whose mutation causes a particularly aggressive type of AML. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.