Studies testing the SGLT2 inhibitors suggest that at least one key benefit of these agents, as illuminated in mouse models of atherosclerosis, for example, is the reduction in circulating and lesional immune and inflammatory signals and oxidative stress, perhaps, in part to increased AMPK signaling and/or reduction in activation of factors such as NF-kB, the NLRP3-caspase-1 inflammasome, and the AGE-RAGE pathways and/or direct effects on immune cell fate [76–79]. Here, AGER is linked to atherosclerosis.