They demonstrated the coamplification of EGFR and its upstream enhancer on ecDNA, where the new enhancer–oncogene contacts contribute to cancer cell growth.240 Considering that no breakpoints were detected between EGFR and its two upstream enhancers, it is suggested that the incorporation of endogenous enhancers is not only advantageous for GBM cell survival, but also required for oncogene selection. Here, EGFR is linked to glioblastoma.