While BCR::ABL1 overexpression predicts TKI-resistant phenotypes [44], imatinib-induced BCR::ABL1 upregulation has been previously reported in CML cell models and is associated with neoplastic attempts to evade cell death [45], with our findings expanding this concept of BCR::ABL1 upregulation as a compensatory mechanism to Ph+ ALL as well. The gene discussed is ABL1; the disease is acute lymphoblastic leukemia.