Our data also suggest a beta-catenin independent way for GAS2DN to inhibit the CML cell growth through affecting the expression of a subset of genes including HNRPDL. Further investigation of the function and the underlying mechanism of GAS2 in CML would benefit the management of the disease, and shed light on the multiple facets of the biological function of GAS2. This evidence concerns the gene HNRNPDL and chronic myelogenous leukemia, BCR-ABL1 positive.