The cardiovascular effects of sodium glucose co-transport 2 (SGLT2) inhibitors have been demonstrated to be quite helpful in recent clinical trials. Both diabetics and non diabetics, as well as those with and without chronic heart failure, have a lower risk of cardiovascular death and hospitalization due to heart failure. It is not quite apparent what mechanism(s) are responsible for these positive outcomes. The cardioprotective effects of SGLT2 inhibition have been hypothesized to be due to a number of processes, including but not limited to the following: reduction of inflammation, improvement of cardiac energy metabolism, reduction of blood pressure, erythropoiesis, prevention of adverse cardiac remodeling, prevention of ischemia/reperfusion injury, inhibition of the Na+/H+-exchanger, inhibition of SGLT1, reduction in hyperuricemia, increase in autophagy and lysosomal degradation, decrease in epicardial fat mass, increase in erythropoietin levels, increase in circulating pro-vascular progenitor cells, decrease in oxidative stress, and improve vascular function. In an attempt to consolidate and rank the mechanisms in relation to clinical event reduction, we examine the benefits and drawbacks of these suggested processes.