The most frequent genetic alterations in lung cancer include mutations in TP53, EGFR (Epidermal growth factor receptor), KRAS, EML4-ALK (echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase) rearrangements, and altered MET (tyrosine-protein kinase Met) signaling, which play critical roles in tumorigenesis of lung cancer, and therefore affecting the clinical sensitivity to targeted therapy [3, 4]. This evidence concerns the gene TP53 and lung carcinoma.