Therefore, the intriguing questions are: 1) how frequent is EGFR amplification in these patients, 2) how p.T790M can drive tumor progression being so low within the tumor; 3) is there another mechanism of resistance in addition to p.T790M, and 4) is p.T790M able to synergize with activating EGFR mutation. The gene discussed is EGFR; the disease is neoplasm.