First, although sequence analysis of individuals with WS shows that ~95% mutations in WRN genes produce frameshift and nonsense mutations that are predicted to result in truncated proteins, people harboring mutations causing a 90% reduction in WRN helicase activity but leaving WRN exonuclease activity intact do not present with the clinical manifestations of WS (Kamath-Loeb et al., 2017). Here, WRN is linked to Werner syndrome.