For example, S100 glial precursor promoter-regulated v-ERBB (an activated member of the EGFR family) transgenic mice develop oligodendrogliomas, which are potentiated in terms of shorter latency and increased malignancy when initiated in mice deficient for both p16 and p19 (Cdkn2a-null mice) [14]. This evidence concerns the gene CDKN2A and oligodendroglioma.