The central role for Smad7 in CRS was demonstrated in a Smad7 deficiency model, which resulted in enhanced ANG II‐induced loss of miR‐29b expression and the promotion of murine cardiac and renal fibrosis through activation of TGF‐β/Smad3 and NF‐kB signaling.202, 203. Here, SMAD3 is linked to renal fibrosis.