While driver mutations (e.g., mutations in KRAS, EGFR, BRAF) are known to initiate tumor development in lung cancer, secondary mutations may promote subclonal evolution such as mutations in TP53 and PIK3CA, which were previously described in KRAS-, BRAF-, and EGFR-mutant lung tumors [25,26]. The gene discussed is TP53; the disease is lung cancer.