p210BCR-ABL-induced decrease in cell viability observed in 32D/TetOff-p210 cells was unexpected because previous studies have shown that p210BCR-ABL activates phosphatidylinositol 3 kinase (PI3K)-Akt pathway to enhance cell growth [18] and Bcl-X transcription, through signal transducer and activator of transcription 5 (STAT5), to inhibit apoptosis in CML cells [19]. This evidence concerns the gene AKT1 and chronic myelogenous leukemia, BCR-ABL1 positive.