Upon accumulating in the nucleus after exogenous addition, T-oligos induce potent DNA damage responses (DDRs), such as cell cycle arrest and apoptosis, which may be mediated by the ataxia telangiectasia mutated (ATM) pathway and its downstream effectors p53, pRb, E2F1, cdk2, and p95/NBS1 in cancer cells [4,5,8,35,40]. Here, NBN is linked to cancer.