We have recently developed a human stem cell model by homozygous depletion of the exons 15 and 16 of WRN alleles, which recapitulates the major cellular defects of WS, including accelerated senescence, growth arrest, telomere attrition, increased DNA damage response, excessive production of inflammatory factors, as well as increased stem cell attrition in the in vivo niche (Zhang et al., 2015). The gene discussed is WRN; the disease is Werner syndrome.