Three possible pathological relationships between SARS‐CoV‐2 and TGF‐β have been proposed: first, viral infection activates TGF‐β secretion by immune cells; second, downregulation of ACE2 receptors by spike protein and elevated levels of Ang‐II enhance intracellular SMAD2, SMAD4, and promote TGF‐β/SMAD signaling; and third, viral N protein interacts with SMAD3 to promote TGF‐β signaling activation (reviewed in Refs. Here, TGFB1 is linked to viral infectious disease.