SHH and Mobius syndrome: Next-generation sequencing of MB tumors have shown that besides amplification of MYC, MYCN, CCND2, and GLI2, mutations in epigenetic regulator, e.g., histone lysine methyltransferase or acetyltransferase (KMT and HAT, also called “writers”); demethylases or deacetylases (KDM, HDAC, also called “erasers”); and members of the polycomb transcriptional repressor complex, PRC2 and PRC1, account for majority of the genetic perturbations in the non-SHH/WNT groups 3 and 4 MBs (Figure 3) [19,122,126].