Somehow surprisingly, among our 23 EGFR-mutated patients treated with erlotinib, 17 showed OR (complete/partial) regardless of the presence of cancer-relevant co-mutations that can potentially represent mechanisms of primary resistance to EGFR-TKIs, because they occurred in genes coding for proteins that either are directly downstream the EGFR or belong to alternative by-pass pathways, as discussed above. The gene discussed is EGFR; the disease is cancer.