At the molecular level, PKD2 deletion promoted insulin secretion by β cells through increasing the expression and activity of L-type Ca2+ channels and subsequently augmenting high glucose- and membrane depolarization-induced Ca2+ influx, implying that downregulation of PKD2 may contribute to hyperinsulinemia and systemic insulin resistance that underlie metabolic disorders [166]. The gene discussed is PKD2; the disease is metabolic disease.