The hypothesis that MYC or MYCN specifically interacts with p53 loss of function was established in recent studies in which Trp53-inactivated murine cerebellar stem or progenitor cells were transformed by forced overexpression of exogenous Myc or Mycn, driving formation of aggressive tumors resembling human medulloblastoma following transplantation into the cerebellum (Kawauchi et al., 2012; Pei et al., 2012). Here, MYC is linked to medulloblastoma.