Animal models of human aging, which display the characteristic diseases associated with aging, provide insight into the cause of such diseases. Recently a transgenic mouse model, called Klotho, with several premature aging phenotypes has been described. They display premature aging phenotypes such as Osteoporosis, age related skin changes, ectopic calcifications, atrophy of genital organs and thymus, emphysema and short life span (1). KL protein associated with the Klotho mutation is a 1014 amino acid long peptide. It has a putative signal sequence at its N-terminus and a single transmembrane domain near its C-terminus, which is postulated to anchor it to the membrane (2). The extracellular domain has two internal repeats, KL-1 and KL-2 which have 20-40% sequence identity to bacterial b-glucosidase of plants and animals and mammalian lactase glycosylceramidase suggesting a role for Klotho in sphingolipid metabolism (2). kl gene expression was observed to be tissue specific. Improvement of systemic aging phenotypes in kl/kl mice occurs even when the exogenous expression was limited to some organs, suggesting that KL associated aging is regulated through a humoral signaling pathway. KL has been reported to be localized on the cell surface when expressed on Cho cells (1). Human kl cDNA is expected to encode a protein of 1012 amino acids and has 86% homology to mouse kl. Alternative splicing produces two isoforms (a full length membrane bound and the secreted form).