A preclinical study in BCR-ABL+ and BCR-ABL-like B-ALL cell lines and primary cells derived from newly diagnosed and relapsed/TKI-resistant BCR-ABL-like ALL patients, found that STAT5 silencing suppressed cell growth, induced apoptosis, and inhibited leukemogenesis [3]. The gene discussed is ABL1; the disease is acute lymphoblastic leukemia.