The findings that N-Myc and GCN5 appear to work together to maintain a progenitor-like state of inhibited differentiation, high cellular metabolism, and rapid proliferation also support a model in which GCN5 may mediate aspects of nervous system tumor formation by excess N-Myc when such a progenitor-like state appears to be “locked in.” Further studies will provide additional insight into the functions of N-Myc and GCN5 in NSC and tumorigenesis. This evidence concerns the gene KAT2A and nervous system neoplasm.