Targeting oncogenic driver mutations, such as sensitizing mutations in the epidermal growth factor receptor gene (EGFR)2, 3 and fusions of echinoderm microtubule‐associated protein‐like 4 (EML4) and anaplastic lymphoma kinase (ALK), rearrangements of the ROS proto‐oncogene 1 (ROS1), the BRAF V600E mutation, and the MET exon 14 skipping, has significantly improved the prognosis of advanced NSCLC, with higher response rates and longer progression‐free survival compared with those achieved with conventional cytotoxic chemotherapy. This evidence concerns the gene EGFR and non-small cell lung carcinoma.