Taken together, our study strongly supports a therapeutic role for SNG inhibitors to complement the effects of TKIs by targeting additional key proteins and pathways, leading to more complete disease eradication for CML and BCR-ABL+ ALL patients, particularly those TKI-resistant patients carrying BCR-ABL mutations. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.