Consistent with the results obtained using imatinib, CFTRinh-172 led to a significant reduction in p-BCR-ABL in both K562 and SUP-B15 cells as well as significant down-regulation oft-BCR-ABL in K562 cells (Figure 3A) but not in SUP-B15 cells (Figure 3C).Notably, imatinib had no effect on CFTR expression but did result in the down-regulation of p-BCR-ABL and classic Wnt/β-catenin signaling, implying that CFTR protein is located upstream of BCR-ABL in the signaling regulatory networks active in Ph+ acute leukemia cells. The gene discussed is ABL1; the disease is acute leukemia.