Therefore, polymorphisms in KCNK17 that increase TALK-2 activity or expression would be predicted to increase type 2 diabetes risk by blunting beta cell glucose-stimulated Ca<sup>2+</sup> influx, limiting GSIS, promoting Ca<sup>2+</sup><sub>ER</sub> leak and elevating basal insulin secretion. The gene discussed is INS; the disease is type 2 diabetes mellitus.