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Over the past decade, remarkable progress has been made in the management of advanced non-small-cell lung cancer (NSCLC), when tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors have been added to the therapeutic armamentarium. Indeed, dramatic responses to epidermal growth factor receptor (EGFR)-TKIs are observed in patients with NSCLC harbouring activating EGFR driver mutations [1, 2]. Unfortunately, all tumours ultimately develop secondary resistance, half of these due to the acquirement of the gatekeeper EGFR T790M mutation [3].
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Bempt et al. (2018) studied this question.
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