The differential effects of Arid2-IR in renal fibrosis and inflammation suggest that Arid2-IR may be a downstream mediator of Smad3 in renal inflammation because mice null for Smad3 are protected against Smad3-mediated fibrosis and NF-κB-driven inflammation in a number of renal diseases [55,56,57]. This evidence concerns the gene ARID2 and kidney disorder.