Although there has been promising data regarding the usage of FLT3 inhibitors in combination with azacytidine for the management of FLT3-ITD+ in AML patients, these inhibitors have not improved survival to the same level as imatinib in managing CML or ATRA in managing acute promyelocytic leukaemia (APL). The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.