On the other hand, several drugs, evaluated mostly in models of type 2 diabetes (T2D), were encouraging in their potential to improve β-cell mass and function either through a mechanism of reduced metabolic toxicity (e.g., SGLT2 inhibitors) or through the replenishment of the β-cell compartment (e.g., GABA). The gene discussed is SLC5A2; the disease is type 2 diabetes mellitus.