EGFR and neoplasm: Comprehensive molecular profiling of NSCLC has defined genetic alterations that drive tumor growth, including somatic mutations in KRAS (32.2 %), EGFR (11.3 %), and NF1 (8.3 %) as well as chromosomal fusion events involving receptor tyrosine kinases (RTKs) such as ALK, ROS1, and NTRK1.