The premature senescence of mitotic cells derived from A-T, HGPS, and NBS patients has been correlated with an increased rate of telomere loss [31,34,38], whereas the mechanism responsible for the premature senescence of WS and G6PD-deficient fibroblasts appears to be different and has been postulated to reflect the accumulation of DNA damage [26,38]. The gene discussed is G6PD; the disease is Nijmegen breakage syndrome.