OBJECTIVE: To explore whether BAX plays a role in the development of Philadelphia chromosome-positive leukemia and related mechanisms. METHODS: Target-gene knockout mice were used as bone marrow cell donors. Retrovirus over-expressing BCR-ABL were packaged. BCR-ABL-induced B-ALL mouse model was established through donor's B cells transfected by the retrovirus and the B cells over-expressing BCR-ABL were given to the receptor mice by tail vein injection. Western blot was used to detect the protein express and flow cytometry was used to analyze the B cell subpopulations in BAX and WT mouse bone marrows. Kaplan-Meier analysis was used to estimate the survival of diseased mice. RESULTS: BAX deletion caused faster development of BCR-ABL-induced leukemia in vitro and in vivo. BCR-ABL increased BCL-2 expression and enhanced BCL-2/BAX heterodimer formation. CONCLUSION The BAX deletion can accelerate the disease progression of BCR-ABL induced B-ALL.