Several clinically used drugs inhibit ENT1 as a secondary mode of action, including rosuvastatin40 and dipyridamole.41 Interestingly, rosuvastatin increases HbA1c in individuals with and without diabetes,42 and dipyridamole increases glycaemia in mice.43 Taken together, these data suggest that therapeutic alterations in purine salvage may produce a clinically significant alteration in HGP via modulation of adenosine receptors. Here, SLC29A1 is linked to diabetes mellitus.