As discussed above, over-expression of Oxr1 in vivo delays neurodegenerative phenotypes driven by a reduction in OS levels and inflammation (Liu et al. 2015) and intravenous delivery of stably transfected human OXR1 in MSCs resulted in a reduction of OS and inflammation in a mouse model of lupus nephritis (Li 2014). This evidence concerns the gene OXR1 and lupus nephritis.