They showed that Mre11ATLD/ATLD mice are not prone to lymphomagenesis in spite of having defective cell cycle checkpoints and chromosomal translocations similar to that of ATM and NSB1 deficiencies, whereas the apoptosis rate was only slightly reduced in comparison to w.t. Tumor latency was modestly reduced in the background of p53 deficiency, although the modest difference observed in the age of death should not be entirely attributed to increased malignancy of the double Mre, p53 mutants as many of them did not exhibit overt malignancy upon necropsy. This evidence concerns the gene ATM and neoplasm.