The phenotype of Bmi1 over expression overlaps with the phenotype observed in Rb deficient mice and absence of medulloblastoma in GFAP-Cre; Bmi1LSL; RbLox/Lox mice, shows that the transgenic Bmi1 over expression is insufficient to functionally inactivate the p19ARF/p53 pathway and indicates that the oncogenic role of Bmi1 is primarily dependent on repression of p16INK4A/Rb. This evidence concerns the gene GFAP and medulloblastoma.