It has been clinically and scientifically proven that in lung cancer, the identification of oncogenic driver mutations (in genes such as epidermal growth factor receptor [EGFR], anaplastic large-cell lymphoma kinase [ALK], c-ros oncogene 1 [ROS1], and vascular endothelial growth factor receptor [VEGFR]) has successfully led to the development of small drug molecules that are specific to the products of these mutated genes with varying degrees of clinical responsiveness [6,7]. This evidence concerns the gene EGFR and lung cancer.