This observation raises the possibility that Ca2+ binding in Fpn serves a regulatory function, and that the activity of Fpn could be limited in conditions of hypocalcemia—specifically, low plasma ionized calcium (i.e., [iCa2+] < 1.0 mM) characteristic of conditions such as primary hypoparathyroidism, chronic kidney disease, and hypomagnesemia (e.g. in the prolonged use of proton-pump inhibitors)29,30. The gene discussed is SLC40A1; the disease is chronic kidney disease.