Since evaluation of the effects of simultaneous Rad54 and Parp-1 inactivation on MB development was prevented by the lack of viable compound mutants, we investigated the inactivation of DNA repair genes in the context of Ptc1 tumor suppression by examining mice with complete abrogation of either Rad54 or Parp-1 function, in combination with heterozygosis of Parp-1 or Rad54, respectively. Here, PARP1 is linked to neoplasm.