In this context, Al-Nedawi et al. found that EGFR and its glioblastoma deletion mutant isoform EGFRvIII could be packaged in EVs, where they could appear in their phosphorylated state, and that they were functional when internalised by recipient cells, increasing downstream MAPK signalling and the expression of oncogenic factors. The gene discussed is EGFR; the disease is glioblastoma.