A common feature of non-small cell lung cancer (NSCLC), the most common histological type of lung cancer, is the presence of somatic activating mutations of KRAS (~30%) accompanied by inactivating mutations of the tumor suppressor TP53 [3,4], leading to activation of pro-proliferative signaling and disruption of G1/S checkpoint machinery, lack of cell cycle arrest in response to DNA-damaging therapies, such as platinating agents (cisplatin, carboplatin) and irradiation: the commonly used treatment approaches for NSCLC without targetable driver mutations [5,6]. This evidence concerns the gene TP53 and non-small cell lung carcinoma.