We found a higher penetrance of pituitary tumors in the Rb deficient mice than in the Bmi1 transgene model which indicates that transgenic Bmi1 expression acts as a predisposing condition facilitating the silencing of the p16INK4A locus or, alternatively, points to an incomplete transcriptional repression of the p16INK4A pathway or could simply reflect the efficiency of Cre-mediated recombination events for the alleles used. This evidence concerns the gene BMI1 and pituitary tumor.