Given the strong evidence from the Karlseder group that cells from WS patients are defective in replicating the telomeric G-rich lagging strand template [162,163], and WRN is found at telomeres where it interacts with members of the shelterin complex [164], it is probable that WRN performs the timely resolution of G4 DNA and removal of T-loops via its coordinate helicase and exonuclease activities to ensure telomere stability in vivo. Here, WRN is linked to Werner syndrome.