First, we examined CHK1 phosphorylation at Ser345 in an isogenic pair of uncorrected and WRN wild-type-corrected (WSWRN) SV40-transformed Werner syndrome (WS) fibroblasts (36), in which ATM (ATMi), ATR (ATRi) or both (ATMi/ATRi) were chemically inhibited. This evidence concerns the gene ATR and Werner syndrome.