Genetic contribution to kidney stone formation has been well recognized, and a number of studies have reported genetic variations of several human genes, including osteopontin (OPN)[5,6], calcitonin receptor (CTR)[7], vitamin D receptor (VDR)[8], urokinase[9], interleukin (IL-1β and IL-Ra)[10,11], E-cadherin[12], androgen-oestrogen receptors (AR and ER)[13], vascular endothelial receptor growth factor (VEGF)[14], and calcium-sensing receptor (CaSR)[15], which associated with KSD with a predominantly hypercalciuria and calcium oxalate kidney stones. The gene discussed is CALCR; the disease is Hypercalciuria.