To determine whether p27Kip1 loss affected medulloblastoma initiation or progression, we generated mice hemizygous for the SmoA1 transgene that were heterozygous (p27wt/-) or nullizygous for p27Kip1 (p27−/−) and examined tumor incidence at two months of age, a time point preceding symptomatic medulloblastoma onset. This evidence concerns the gene CDKN1B and neoplasm.