In the osteoarthritis (OA) model induced by sodium iodoacetate, activated α7 nAChRs have been shown to inhibit the expression of the OA marker matrix metalloproteinase-9 (MMP-9) and the translocation of NF-kB from the cytoplasm to the nucleus by enhancing the phosphatidylinositol 3-kinase (PI3K)/serine/threonine-protein kinase (Akt) signaling pathway, thereby alleviating pain [51]. The gene discussed is AKT1; the disease is osteoarthritis.