In contrast, the GTML model, our previously characterized GEMM for medulloblastoma also driven by MYCN, more closely resembled group 3 medulloblastoma (Figures 2C and 2D), a subgroup of medulloblastoma associated more commonly with amplification of CMYC. Furthermore, while GTML tumors showed much fewer regions of hypermethylation than human medulloblastoma patient tumors (Diede et al., 2013), the human WTC10 MYCN tumors exhibited DMRs at almost half the sites found in patient-derived tumors (Figure 2A). This evidence concerns the gene MYC and medulloblastoma.