Survivin is a member of the inhibitor of apoptosis family of proteins and functions to inhibit apoptosis and promote cell division.Survivin expression is developmentally regulated in normal tissue, with little expression in most terminally differentiated tissues. The abnormally high expression of survivin in cancer cells makes it an attractive anticancer target. However, accumulating evidence indicates potential functions for survivin in normal tissues, indicating that survivin expression is not cancer specific. Interestingly, survivin expression is upregulated by adipokines such as leptin, suggesting that the molecular effects of adiposity on carcinogenesis might be mediated by suppression of apoptosis through survivindependent mechanisms. Moreover, it has been demonstrated that survivin is regulated by cytokines in lymphocytes and plays an important role in proliferation and survival of hematopoietic cells. To our knowledge, no studies have examined the impact of obesity on survivin expression. We hypothesized that an obese environment could promote survival of the ASC niche by decreasing its sensitivity to apoptosis via a survivindependent mechanism. We show for the first time that circulating levels and WAT expression of survivin are increased in human obesity. Furthermore, we demonstrate that survivin protein expression is elevated in ASCs isolated from obese individuals, and protects from apoptosis. These findings outline a regulatory for survivin as a new player in AT remodeling with potential impact in the mechanisms linking obesity/adiposity to increased cancer risk.