In such cases, deletion of the tumor suppressor gene phosphatase and tensin homolog (PTEN) was found to accelerate the development of CML, as recipient mice receiving cells transduced from bone marrow (BM) of Ptenfl/fl mice with BCR-ABL-Cre-GFP retrovirus developed CML at a faster rate than those receiving cells transduced with the corresponding BCR-ABL-GFP control retrovirus, while overexpression of PTEN consequently delayed CML development [52]. This evidence concerns the gene PTEN and chronic myelogenous leukemia, BCR-ABL1 positive.