A method to select a cancer patient who is predicted to benefit or not benefit from therapeutic administration of an EGFR inhibitor, comprising: a) detecting in a sample of tumor cells from a patient a gene copy number change selected from the group consisting of: i) amplification of the epidermal growth factor receptor (EGFR) gene; ii) polysomy of the EGFR gene; iii) amplification of the human tyrosine kinase receptor type receptor gene; and iv) polysomy of the HER2 gene; b) comparing the EGFR and/or HER2 gene copy number in the patient's tumor cell sample to EGFR and/or HER2 gene copy number from tumor cells that are sensitive to or resistant to an EGFR inhibitor and c) selecting the patient as being predicted to benefit from therapeutic administration of the EGFR inhibitor, if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically similar to or greater than the EGFR and/or HER2 gene copy number in tumor cells that are sensitive to an EGFR inhibitor, or if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically greater than the EGFR and/or HER2 gene copy number in tumor cells that are resistant to an EGFR inhibitor; or d) selecting the patient as being predicted to not benefit from therapeutic administration of the EGFR inhibitor, if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically less than the EGFR and/or HER2 gene copy number in tumor cells that are sensitive to an EGFR inhibitor, or if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically similar to or less than EGFR and/or HER2 gene copy number in tumor cells that are resistant to an EGFR inhibitor. a) detecting in a sample of tumor cells from a patient a gene copy number change selected from the group consisting of: i) amplification of the epidermal growth factor receptor (EGFR) gene; ii) polysomy of the EGFR gene; iii) amplification of the human tyrosine kinase receptor type receptor gene; and iv) polysomy of the HER2 gene; i) amplification of the epidermal growth factor receptor (EGFR) gene; ii) polysomy of the EGFR gene; iii) amplification of the human tyrosine kinase receptor type receptor gene; and iv) polysomy of the HER2 gene; b) comparing the EGFR and/or HER2 gene copy number in the patient's tumor cell sample to EGFR and/or HER2 gene copy number from tumor cells that are sensitive to or resistant to an EGFR inhibitor and c) selecting the patient as being predicted to benefit from therapeutic administration of the EGFR inhibitor, if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically similar to or greater than the EGFR and/or HER2 gene copy number in tumor cells that are sensitive to an EGFR inhibitor, or if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically greater than the EGFR and/or HER2 gene copy number in tumor cells that are resistant to an EGFR inhibitor; or d) selecting the patient as being predicted to not benefit from therapeutic administration of the EGFR inhibitor, if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically less than the EGFR and/or HER2 gene copy number in tumor cells that are sensitive to an EGFR inhibitor, or if the EGFR and/or HER2 gene copy number in the patient's tumor cells is statistically similar to or less than EGFR and/or HER2 gene copy number in tumor cells that are resistant to an EGFR inhibitor.