The same group showed, in a rat model of hyperoxaluria, differential renal expression in the pathways related to OS (including upregulation of NADPH oxidase subunits Nox2, Nox4 and P22phox, and Gpx2), KIM-1 (a marker of renal injury), crystallization modulators (upregulation of OPN, MGP, Fetuin B, CD44, Clusterin, Bikunin/AMBP) and to osteogenesis (upregulation of Runx1, Runx2, KRT18, KRT8, and THP downregulation) [83]. This evidence concerns the gene FMO5 and Hyperoxaluria.