In numerous cancers, including glioblastomas, colon cancer, breast cancer, and non-small cell lung cancer, the output of the EGFR pathway is commonly increased by genetic mutation and overexpression of the receptor, overactivity of its ligands or cofactors and less commonly reduced inhibition through loss of its negative regulatory pathways driving the mitogenic, antiapoptotic, angiogenic and pro-invasive behaviour of the cancer cells. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.