In-vitro and animal experiments have shown that coculture of ADSCs and HS-sourced Fbs reduces the proliferation ability of HS-sourced Fbs, decreases the expression of TGF-β1, phosphorylated Smad2/3, and type I/III collagen in the TGF-β1/Smad pathway, blocks the interaction between TGF-β1 and Smad3 and subsequent translocation of Smad3 to the nucleus, and reverses the TGF-β1 and Smad3 signal transduction pathway through crosstalk with other transduction pathways, thus preventing ECM deposition, tissue fibrosis, and pathologic scar formation [12, 13]. The gene discussed is SMAD3; the disease is fibrosis.