Further study reveals that Arid2-IR mediates renal inflammation via the NF-κB-dependent mechanism and thus Arid2-IR may be a downstream mediator of Smad3 and functions to promote NF-κB-driven renal inflammation without effect on TGF-β/Smad3-mediated renal fibrosis in a mouse model of obstructive nephropathy and in vitro103. This evidence concerns the gene TGFB1 and renal fibrosis.