Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
Example: In 1582 the united provinces invited francis, duke of anjou to lead them; but after a failed attempt to take antwerp in 1583, the duke left the netherlands again. after the assassination of william of orange (10 july 1584), both henry iii of france and elizabeth i of england declined the offer of sovereignty. however, the latter agreed to turn the united provinces into a protectorate of england (treaty of nonsuch, 1585), and sent the earl of leicester as governor-general. this was unsuccessful and in 1588 the provinces became a confederacy. the union of utrecht is regarded as the foundation of the republic of the seven united provinces, which was not recognized by the spanish empire until the peace of westphalia in 1648.
Example solution: In what year did francis, duke of anjou leave the netherlands?
Example explanation: The generated question is perfect. Because the question is based on second sentence of the input passage and its answer is 1583.

Problem: Mutations of the epidermal growth factor receptor (EGFR) gene have been reported in non-small-cell lung cancer (NSCLC), especially in patients with adenocarcinoma and never smokers. Some common somatic mutations in EGFR, including deletion mutations in exon 19 and leucine-to-arginine substitution at amino acid position 858 (L858R) in exon 21, have been examined for their ability to predict sensitivity to gefitinib or erlotinib, which are selective EGFR tyrosine kinase inhibitors (EGFR-TKIs). On the other hand, reports have shown that the threonine-to-methionine substitution at amino acid position 790 (T790M) in exon 20 is related to gefitinib resistance. Some studies have indicated that high copy numbers of the EGFR gene may be a more effective molecular predictor to responsiveness and prolonged survival in patients treated with EGFR-TKIs. Here, we describe two NSCLC patients with the L858R mutation who did not respond to gefitinib. Case 1 harbored both the T790M and L858R mutations, and fluorescence in situ hybridization showed EGFR gene amplification. Case 2 harbored both the L858R and aspartic acid-to-tyrosine substitution at amino acid position 761 in exon 19 of EGFR mutations and had a high polysomy status for EGFR. In these two cases, tumors showed resistance to gefitinib treatment despite the presence of EGFR L858R mutation and increased copy number. Our findings encourage further molecular analysis to elucidate the relationship between the EGFR status, including mutations and amplifications, and the responsiveness of NSCLC to gefitinib.

Solution: Mutations in which gene determine response to both erlotinib and gefitinib?