Both PGE2 production and EP3 expression have previously been shown to contribute to βcell dysfunction in the BTBR LeptinOb mouse model, a unique and robust model of T2D, as well as human islets isolated from T2D human organ donors.3 In the current work, islet PGE2 synthetic gene expression and PGE2 excretion are both unchanged in NGOB or HGOB islets vs. WT on the C57Bl/6J background (Figure 1e,f), suggesting agonist-sensitive EP3 signaling does not contribute to either β-cell compensation or β-cell failure in this model. The gene discussed is PTGER3; the disease is type 2 diabetes mellitus.