This observation suggests that cellular calcium concentration is an important regulator of calbindin-D28K-expression, overriding the stimulatory effects of vitamin D. The reduction in calbindin-D28K-expression coupled with the probable mislocalisation of TRPV5-S682P in DCT tubules could result in reduced calcium reabsorption, and thus explain the hypercalciuria observed in Trpv5682P/682P and Trpv5682P/+ mice. The gene discussed is CALB1; the disease is Hypercalciuria.