Two different NSCLC tumour models with distinct molecular defects (A549: K-Ras (G12S) oncogenic mutant and truncated LKB1-null but wild-type p53 vs H1299: p53-null, wild-type K-Ras and LKB1) were used to examine whether detected chronic response of the AMPK-p53/CDKIs and Akt-mTOR pathways to IR apply in lung cancer types with diverse oncogenic genotypes. This evidence concerns the gene KRAS and neoplasm.