As SARS‐CoV N protein is able to interact with Smad3 and activate TGF‐β/Smad3 signaling to promote fibrosis response,[8] we thus hypothesized that SARS‐CoV‐2 N protein may be able to trigger Smad3 signaling to induce TEC death and AKI via the Smad3‐dependent G1 cell cycle arrest mechanism, and targeting Smad3 may be a novel and specific therapy for SARS‐CoV‐2‐associated AKI. Here, TGFB1 is linked to acute kidney injury.