Here, we have shown that genetic loss of Atmin or Atm reduces GBM formation initiated by deletion of Trp53. This finding indicates that Atm/Atmin is crucial for Trp53-deficient GBM development, and suggests the use of ATM inhibitors, which have already been developed, for GBM therapy (Basu et al., 2012; Golding et al., 2009; 2012; Batey et al., 2013). The gene discussed is ATM; the disease is glioblastoma.