However, as it has been well established that Ang II acts via AT1 to activate NF‐κB‐driven inflammation and Smad3‐dependent fibrosis, the marked differences in AT1‐associated TGF‐β/Smad3‐mediated renal fibrosis and NF‐κB‐dependent renal inflammation in response to Ang II as seen in the present study remained meaningful. The gene discussed is NFKB1; the disease is renal fibrosis.