EGFR and neoplasm: In contrast, tumor cells have evolved mechanisms to constitutively activate EGFR signaling by (1) EGFR overexpression (leading to ligand-independent activation), (2) acquisition of constitutively activating EGFR mutations, and/or (3) secretion of EGFR ligands,2,22,23,24,25,26,27,28 which results in basal EGFR activation and, as a consequence, a range of cellular outcomes, such as proliferation and resistance to apoptosis.3