For example, activating mutations in the Kirsten rat sarcoma viral oncogene homolog (KRAS) and epidermal growth factor receptor (EGFR) genes and rearrangements in the anaplastic lymphoma kinase (ALK) or ROS proto-oncogene 1 receptor tyrosine kinase (ROS1) genes are identified as oncogenic drivers in certain subtypes of NSCLC [43,44,45,46,47], so are the inactivating mutations in tumor protein p53 (TP53) and retinoblastoma 1 (RB1) genes in SCLC [48,49]. This evidence concerns the gene ALK and non-small cell lung carcinoma.