For example, in a recent study, a recurrent driver mutation named EGFRvIII—which encodes a truncated, constitutively active epidermal growth factor receptor (EGFR)—was shown to activate and repress thousands of enhancer-associated genes involved in glioblastoma development.22 This EGFRvIII-dependent reprogramming of the epigenetic landscape is, inlarge part, due to the ability of this oncogene to activate the expression of two TFs, SOX9 and FOXG1. The gene discussed is EGFR; the disease is glioblastoma.