We previously generated a mouse model with a deletion of part of the helicase domain of the murine WRN homologue (referred as WrnΔhel/Δhel mice hereafter) [14] that recapitulates many of the WS phenotypes, including an abnormal hyaluronic acid excretion, higher reactive oxygen species (ROS) levels, dyslipidemia, increased genomic instability, and cancer incidence [15, 16]. This evidence concerns the gene WRN and Werner syndrome.