EGFR inhibition causes significant increases in TNF-α expression, with subsequent signaling through TNFR1 and activation of JNK and ERK resulting in enhanced GBM survival; inhibition of TNF, JNK and/or ERK signaling sensitizes GBM cells to EGFR inhibition both in vitro and in vivo [391, 392]. The gene discussed is EGFR; the disease is glioblastoma.