Both activities were first believed to be tumor-specific autocrine growth factors, and intriguingly TGF-α, but not TGF-β, competed for the binding of 125I-EGF to specific, saturable high-affinity binding sites on cells known as the EGF receptor (EGFR) [14,15], which also binds to heparin-binding EGF-like growth factor (HB-EGF), betacellulin, amphiregulin, and epiregulin [16]. The gene discussed is EGF; the disease is neoplasm.