Our team has focused on fortilin, a 172-amino acid polypeptide with multiple biological functions. Fortilin binds p53, a tumor suppressor protein, and prevents it from transcriptionally activating its target pro-apoptotic genes, such as BAX and PUMA. In addition, fortilin negatively regulates IRE1α, an ER-stress handling molecule and protects cells against ER-stress induced apoptosis. Fortilin fortifies cells against oxidative stress by binding and keeping peroxiredoxin-1 (PRX1) from inactivated by phosphorylation. We are interested in the role of fortilin in stem cell preservation and differentiation. We hope to use fortilin, through gene transfer and other overexpression strategies, to preserve and maximally utilize various stem cells to treat chronic human diseases, such as heart failure, Alzheimer’s disease, and diabetes mellitus.