A possible explanation for the lower mutation burden is that mouse tumors are established in a Trp53-null background and either MYC overexpression in G3 MBs, PTCH1 mutation in SHH MBs or B-CATENIN mutation in WNT MBs, all of which are found in corresponding human MB subgroups and sufficient to induce tumor development thus negating the requirement for additional driver mutations. Here, PTCH1 is linked to neoplasm.