Our results suggest that genes involved in NSE activation and natural variants modulating NSE inclusion (Figs 1, 2c–f and 4h) could modify the phenotypic complexity of A-T and also A-T heterozygotes who lack overt clinical features but may display increased radiosensitivity and cancer risk50, ie. phenotypes influenced by the critical U2AF-regulated pathway in the ATM signalling network (Fig. S2). This evidence concerns the gene ATM and cancer.