In NRK-52E cells from rat proximal tubular epithelium, oxalate exposure (0–1 mM) promoted mitochondrial changes and an imbalance of the NADPH oxidase subunits Nox4/1 (protective role) vs. Nox2 (kidney injury) [56], which is known to underlie the pathophysiology of hyperoxaluria due to significant production of reactive oxygen species (ROS) [57]. This evidence concerns the gene FMO5 and Hyperoxaluria.