Given the link between many of these regulators and processes that control cellular growth, survival, and motility, it is not surprising that oncogenic pathways, such as those triggered by mutant EGFR, MET, K-ras, AKT, and the loss of tumor suppressors, including p53 or PTEN, influence the nature and composition of tumor-derived EVs. This evidence concerns the gene EGFR and neoplasm.