We previously generated a mouse model with a deletion in the helicase domain of the murine WRN homologue (hereafter referred as WrnDhel/Dhel) [14] that recapitulates most of the WS phenotypes, including an abnormal hyaluronic acid excretion, higher reactive oxygen species (ROS) levels, dyslipidemia, increased genomic instability, and cancer incidence. The gene discussed is WRN; the disease is Werner syndrome.