Tumor sensitivity to EGFR inhibitors is observed despite the fact that these tumors harbor no mutation or amplification of the Egfr locus; moreover, comparable phenotypes observed following treatment with EGFR-specific inhibitors (gefitinib, erlotinib) or a pan-Erbb inhibitor (CI-1033) indicate that EGFR is likely the functionally predominant Erbb tyrosine kinase in this model of PNET tumorigenesis. This evidence concerns the gene EGFR and neoplasm.