By crossing both, type A (Asp140Gly) and B (disruption of exon 3 to 9) mouse models, double heterozygous mice (Slc3a1+/-Slc7a9+/-) have been generated to determine if partial loss of function of one of those proteins and digenic inheritance of cystinuria-related genes could induce urolithiasis in mice. This evidence concerns the gene SLC7A9 and cystinuria.