In human breast cancer cells, Adriaens et al. showed that treatment with the p53-inducer Nutlin-3 induces NEAT1 expression levels in association with an increase in PSs formation; at the same time, they found that NEAT1 silencing leads to accumulation of DNA damage and to induction of DDR signaling, as confirmed by the enhancement in γH2AX (Histone H2AX) levels and DNA damage foci formation, as well as the increase in the phosphorylated fraction of KAP1 (KRAB-associated Protein 1), known to be an ATM (ataxia-telangiectasia mutated kinase) substrate [3]. Here, NEAT1 is linked to breast carcinoma.