Our study is the first to show how CFTR protein regulates the activity of PP2A in Ph+ acute leukemia cells, whereas the other two studies did not report this effect: high CFTR expression inhibited the phosphatase activity of PP2A to protect and maintain the continuous activation of BCR-ABL and classic Wnt/β-catenin signaling via the interaction with PP2AA subunit in the cytosol of Ph+ acute leukemia cells; The persistent activation of BCR-ABL further inhibited the anti-leukemia activity of PP2A, creating a feedback loop promoting CML-BC transformation and the progression of Ph+ B-ALL. The gene discussed is CFTR; the disease is breast cancer.