Hyperglycemia is the primary factor responsible for the microvascular, and to lesser extent, macrovascular complications. Despite this well established relationship, approximately half of all type 2 diabetic patients in the US have a HbA1c≥7.0%. In part, this is associated with the side effects, i.e. weight gain and hypoglycemia, of currently available antidiabetic agents and in part by the failure to utilize medications that reverse the basic pathophysiologic defects present in patients with type 2 diabetes. The kidney has been show to play a central role in the development of hyperglycemia by excessive production of glucose throughout the sleeping hours and enhanced reabsorption of filtered glucose by the renal tubules secondary to an increase in the threshold at which glucose spills into the urine. Recently, a new class of antidiabetic agents, the sodium-glucose cotransporter 2 (SGLT2) inhibitors, has been developed and approved for the treatment of patients with type 2 diabetes. In this review, we examine their mechanism of action, efficacy, safety, and place in the therapeutic armamentarium. Since the SGLT2 inhibitors have a unique mode of action that differs from all other oral and injectable antidiabetic agents, they can be used at all stages of the disease and in combination with all other antidiabetic medications.