In a previous exploratory study of 197 consecutive NSCLC cases with TKI-sensitive EGFR-mutations, 11 exhibited primary resistance to EGFR-TKIs, but apart from three of these cases exhibiting either concomitant p.T790M, MET-amplification, or ALK-fusion, no other co-mutations in driver genes that could explain the intrinsic TKI-resistance were identified by targeted NGS [25]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.