As it can easily be envisaged that beta-cell dysfunction and death in diabetes involves increased intracellular levels of adenosine and/or 2’-deoxyadenosine, it is tempting to propose that a pharmacological strategy to reduce beta-cell adenosine, for example via increased ADA1 activity, could lead to improved beta-cell function and survival in both T1D and T2D. This evidence concerns the gene ADA and type 1 diabetes mellitus.