Therefore, by using a gene-dosage model of NBS1, we demonstrated that the role carried out by the MRN complex in cancer is strictly dependent on the amount of NBS1 protein expressed, which presumably determines how much RS-induced DNA damage is accumulated/induced, how much p53 can be functionally activated and, consequently, how many lesions can be tolerated without provoking apoptosis (Figure 5). This evidence concerns the gene NBN and cancer.