Specifically, we examined whether SNG inhibitors plus a TKI, to dually inhibit the BCR-ABLTyr177-mediated GRB2-RAS-MAPK pathway in addition to BCR-ABL activity, might be a promising treatment for CML/ALL patients unlikely to respond to TKI monotherapies, as it could more effectively reduce the CML/ALL stem cell burden, and avoid the development of TKI-resistance and disease relapse. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.