These results identified the Sp1-BCR/ABL axis as a new molecular regulator underlying the anti-cancer actions of BORT and are in line with our previous discoveries in AML [19, 20, 24] showing that BORT treatment disrupts Sp1-dependent KIT/FLT3 kinase signaling, DNA hypermethylation and restores miR-29b expression. The gene discussed is ABL1; the disease is acute myeloid leukemia.