Our data also show that the obese microenvironment in SAT determines survivin protein levels in hASCs via several mechanisms including post-transcriptional and post-translational control of gene expression, as previously reported in cancer cell lines.21 Although several strategies have been developed to target survivin in cancer therapy,61 our study in hASCs suggests that simply turning off the survivin transcriptional machinery will not be sufficient to decrease survivin levels and increase the apoptotic sensitivity of obese hASCs. Here, BIRC5 is linked to cancer.