That T-oligos substitute for exposure of the telomere 3' overhang as a stimulus for DNA damage-like signaling is further suggested by the recent demonstration that WRN, the protein mutated in Werner syndrome [72] and known to localize to the telomere and to resolve the telomere loop structure [73,74], is required for T-oligo initiated signaling [15]. The gene discussed is WRN; the disease is Werner syndrome.