Multiple resistance mechanisms have been described, involving three mechanisms: altered drug target, bypass track activation, and morphological alterations.2 The most frequent drug target alteration is the T790M mutation that accounts for 50–60% of secondary resistance to first and second generation EGFR TKI therapies.2 Based on phase III data, osimertinib (a third generation EGFR TKI) is the preferred treatment for patients whose tumour is T790M positive after progression on a first or second generation EGFR TKI.3 The gene discussed is EGFR; the disease is neoplasm.