Therefore, further molecular analysis of wild-type EGFR NSCLC might identify additional driver oncogenes (i.e., anaplastic lymphoma kinase [ALK], c-ros oncogene 1 [ROS1] or rearranged during transfection [RET] rearrangement, proto-oncogene protein c-met [MET] amplification, human epidermal growth factor receptor 2 [HER2] mutation or amplification, v-Raf murine sarcoma viral oncogene homolog B1 [BRAF] mutation, fibroblast growth factor receptor 1 [FGFR1] amplifications, and discoidin domain receptor-2 [DDR2] mutations) and provide alternative targeted therapies. This evidence concerns the gene EGFR and non-small cell lung carcinoma.