Additionally, in a model of mouse with excisional wound, human AF-MSCs significantly enhanced wound healing via the TGF-beta/SMAD2 pathway [95], while human AF-MSCs accelerated wound closure through TGF-β/SMAD2 and PI3K/Akt pathways under the condition of hypoxia [96]. The gene discussed is SMAD2; the disease is atrial fibrillation.