Diabetes is a disorder of complex interaction between genetic susceptibility and environmental perturbation. Various epigenetic models, such as intra-uterine growth retardation, have been shown to contribute to pancreatic beta-cell dysfunction. More recently, beta-cell dedifferentiation has been discovered as a mechanism for beta-cell dysfunction in diabetic mouse model. The project aim to understand the role of classic epigenetic modules in regulating beta-cell identity and function in human context. We’ll survey changes in histone modifications across human pancreas samples over various age groups and diabetic conditions. Understanding how histone modification changes with age and disease state in human will enable the research community to identity factors that underlie aging related decline in beta-cell function and identity.