In lung cancer, considerable progress in developing molecularly-driven therapeutics has been made in the past decades, mainly including targeted therapies against oncogenic drivers, such as EGFR, HER2, EML4-ALK, MET, ROS1, and BRAF mutations, and immunotherapies in non-oncogene-driven lung cancer, such as PD1 and PDL1 alterations (5, 6). This evidence concerns the gene EGFR and lung cancer.