Obesity, insulin resistance, and genetic susceptibilities are among the common antecedent of both GDM and T2D.2,3 Adenosine deaminase (ADA; EC 3.5.4.4), a key enzyme in purine metabolism, regulates extracellular and intracellular concentrations of adenosine by irreversible deamination of adenosine into inosine.4 The role of ADA has been implicated as an important regulator of insulin action and in the pathogenesis of diabetes mellitus. Here, ADA is linked to obesity due to melanocortin 4 receptor deficiency.