The identification of genetic risk factors, as mutations in somatic and germ cells (EGFR, TP53, KRAS, BRAF, ERBB2, MET, STK11, PIK3CA), gene amplifications (EGFR, ERBB2, MET, PIK3CA, and NKX2), deletions (DOK2) (Berger et al., 2010), and presence of fusion genes (ALK/EML4) (Soda et al., 2007), have allowed to develop specific treatments, but although they increase the susceptibility to develop lung cancer (Braun et al., 1994), they have not shown a concordance with the mortality rates because their limited ability to treat patients only with the associated risk factor (Blanchon et al., 2006). This evidence concerns the gene EGFR and lung carcinoma.