In particular, by measuring the percentage of mitotic cells in which p53 colocalizes with the centrosomes in lymphoblastoid cell lines (LCLs) and in cell cycle-reactivated peripheral blood mononuclear cells (PBMCs), we have been able to discriminate healthy individuals (i.e., wild-type ATM alleles; p53-MCL > 75%) from Ataxia-Telangiectasia (A-T) patients (i.e., biallelic ATM mutations; p53-MCL < 30%) and from A-T healthy carriers (i.e., monoallelic ATM mutations; p53-MCL > 40% < 60%)29,32. This evidence concerns the gene ATM and Ataxia-telangiectasia.