MYC and Mobius syndrome: 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.