In combination with the aggressive pathology observed in early tumors from SmoA1 mice lacking p27Kip1, the higher tumor incidence in Ptc1+/− mice lacking p27Kip1 further confirms that p27Kip1 is haploinsufficient in Shh-mediated medulloblastomas and that its loss of function contributes to medulloblastoma progression. Here, CDKN1B is linked to medulloblastoma.