Thus, functional inactivation of PP2A by increased BCR/ABL kinase activity seems to be required for the transduction of aberrant mitogenic, survival and antidifferentiation signals, and for the post-translational enhancement of BCR/ABL expression and oncogenic activity in CML-BCCD34+ marrow myeloid progenitors (Figure 1). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.