Biallelic loss-of-function mutations in SLC34A1 cause idiopathic infantile hypercalcemia (IIH) resulting from renal phosphate wasting, decreased circulating FGF-23 levels and increased 1,25 (OH)2 vitamin D3 production, causing a phenotype of hypercalcemia, hypercalciuria and nephrocalcinosis17,22. This evidence concerns the gene SLC34A1 and hypercalcemia disease.