AKT1 and glioblastoma: reported that the oncogenic receptor tyrosine kinase EGFRvIII was transferred to EGFR-negative endothelial cells and to A431 cells, which express only the wild-type EGFR, via microvesicles derived from EGFRvIII-positive glioblastoma cells, resulting in the activation of downstream signaling pathways such as the mitogen-activated protein kinase (MAPK) and Akt pathways (28).