The validation of ATM inhibition in the tumor by p(S1981)ATM and KI67 immunostaining under our experimental conditions (Fig. 5), supports this opinion and indicates the following three reasons as more likely explaining the discrepancy with results reported by Biddlestone-Thorpe and coworkers17: first, the nature and extent of the TP53 deficiency in the orthotopic tumors used in the two studies have probably contributed to the differences. Here, ATM is linked to neoplasm.