KRAS mutation promotes post-irradiation cell survival through EGFR activity in non-small-cell lung cancers (NSCLC) as demonstrated in NCI-H1703 cells in vitro and in vivo[13], [14] and possibly through wild-type HRAS, which has been shown in DLD-1 colorectal and MiaPaCa-2 pancreatic cancer cells harboring frequent mutations in KRAS [15]. This evidence concerns the gene HRAS and non-small cell lung carcinoma.