After disease progression on first-generation EGFR-TKIs, the acquired resistance mechanisms in this study are consistent with the published data [19], including EGFR T790M mutation, MET amplification, ERBB2 amplification, activation of EGFR downstream signaling, and histological transformation to small-cell or squamous cell carcinoma, even sarcomatoid carcinoma, and so on. This evidence concerns the gene EGFR and squamous cell carcinoma.