Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic β-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca(2+) channels (VDCC). The subsequent rapid rise in cytoplasmic free Ca(2+) concentration triggers insulin exocytosis. However, despite more than 40 years of investigation, certain aspects of the intracellular Ca(2+) responses to glucose and secretagogues remain unexplained, suggesting the involvement of additional Ca(2+) channels. Here, we discuss the emerging role of store-operated Ca(2+) channels carried by Orai1 and transient receptor potential canonical 1 (TRPC1) proteins and regulated by the stromal interaction molecule 1 (STIM1) in the control of glucose-induced insulin secretion. The role of other voltage-independent cation channels formed by other members of the TRP channels family is also addressed.