To define the gene circuits that are deregulated during gliomagenesis in a PRC2-dependent manner, we used a well-established mouse model of gliomagenesis that relies on the loss of Ink4a/Arf combined with the overexpression of the constitutively active mutant form of the human epidermal growth factor receptor (EGFR) known as EGFR variant III (hereafter indicated as EGFR*), the two most common lesions in human high-grade gliomas (HGGs)32 (Fig. 1a and Supplementary Fig. 1a). The gene discussed is EGFR; the disease is glioma.