ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: Despite this, CML cells acquiring non-genetic imatinib resistance mechanisms may still respond to higher-generation tyrosine kinase inhibitors (TKI), suggesting that cell plasticity is constrained around BCR-ABL1 and that the emerging different phenotypes may still rely on the kinase or scaffolding activity of BCR-ABL1 [19].