Furthermore, selective inhibition of Nox1 and Nox2 subunits reduced augmented NADPH-dependent superoxide levels in the renal cortex and improved endothelial relaxations in arteries from the hyperoxaluric group, which suggests that Nox1 and Nox2 are key pathogenic sources of ROS-mediated renal endothelial dysfunction associated to hyperoxaluria. This evidence concerns the gene CYBB and Hyperoxaluria.