The downregulation of cyclin D3 due to infiltration is causally related to beta cell dysfunction and beta cell-apoptosis in beta cells from NOD mice. We would like to confirm whether this is true in human beta cells. In order to validate cyclin D3 as a target for T1D therapy in humans, we need to evaluate the impact of inflammation on the expression levels of cyclin D3 in pancreatic beta cells from individuals at risk of developing T1D, newly diagnosed T1D patients and, non-medalist overtly diabetic patients, in comparison to control individuals, as an approach to study the disease in humans in relationship to cyclin D3 expression levels, as we have observed in NOD mice.