SLC7A9 and cystinuria: Moreover, when a type AB cystinuria mouse model was generated upon crossing Slc3a1−/− mice with Slc7a9−/− mice, the double heterozygous mice (Slc7a9+/-/Slc3a1+/-) exhibited lower expression of system b0,+ and higher hyperexcretion of cystine than the single heterozygotes (Slc7a9+/-/Slc3a1+/+ and Slc7a9+/+/Slc3a1+/-), giving rise to lithiasis, thus showing that cystinuria has a digenic inheritance in this mouse model (Espino et al. 2015).