This approach provided compelling evidence that differences in drug response can be pattern clustered in patient groups of interest and reveals patient-to-patient variation.8 For example, the authors identified a subset of patients with T-ALL without ABL1 mutations or fusions responsive to dasatinib inhibition, suggesting an indirect mechanism of sensitivity to dasatinib-based therapy.8 The gene discussed is ABL1; the disease is acute lymphoblastic leukemia.