Werner syndrome (WS) ("Progeria of the adult"; entry *27770 (1)) was originally defined by Dr. Otto Werner in 1904 on the basis of "scleroderma-like" thin, tight skin and bilateral cataracts in a sibship (2). Among the many systemic clinical features of WS, the various progeroid features have drawn special attention. WS is caused by a mutation at the Werner syndrome gene (WRN) locus, which belongs to the family of RecQ helicases (GenBank accession number L76937)(3). This review focuses on the comparative aspects of WRN, including differential gene action within humans and the potential differences between species, particularly the mouse and human.