Disruption of CML cell-BMSC adhesion, using an N-cadherin antagonist peptide (containing the HAV sequence) or the N-cadherin function-blocking antibody GC-4 increased CML cell sensitivity to the tyrosine kinase inhibitor imatinib [130, 131]. The gene discussed is GC; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.