However, Eiring et al. demonstrated that leukaemic cells maintained their cytoplasmic β-catenin expression despite BCR::ABL1′s inhibition by imatinib, suggesting that β-catenin expression was decoupled from BCR::ABL1 and contributed to intrinsic TKI resistance in CML cells [55]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.