For example, anticancer agents blocking oncogenic EGFR (e.g., dacomitinib, canertinib) stimulated the release of EVs carrying EGFRvIII and genomic DNA in glioblastoma animal models and patients (Skog et al., 2008; Montermini et al., 2015; Choi et al., 2019), and in turn, EV-EGFRvIII were shown to fuse with cancer cells lacking EGFRvIII and transfer the oncogenic activity (Al-Nedawi et al., 2008). Here, EGFR is linked to cancer.