However, NSCLC patients initially response to these EGFR-TKIs almost invariably develop drug resistance [4, 5], which commonly arise through the acquisition of a second-site mutation (T790 M) within EGFR, or via activation of compensatory signaling pathways that bypass receptor and restore downstream oncogenic signaling [6, 7]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.