,7 In patients with EGFR-mutant NSCLC, the alterations in MET signaling, including MET gene amplification (METamp) and MET overexpression, are significant mechanisms of acquired resistance to EGFR TKIs, through the activation of EGFR-independent phosphorylation of ErbB3 and downstream activation of the PI3K/AKT pathway.8 Here, EGFR is linked to non-small cell lung carcinoma.