Overexpression of EGFRvIII in human GBM cells results in constitutively active receptor expression and enhances tumorigenicity in nude mice, to a significantly greater extent than overexpression of wild‐type (wt) EGFR 5, 6, which is mediated by both an increase in proliferation and a decrease in apoptosis of tumor cells 7, as well as inducing angiogenesis and conferring chemoresistance that is associated with upregulation of anti‐apoptotic Bcl‐XL7, 8, 9. The gene discussed is EGFR; the disease is glioblastoma.