The absence of Smad7 results in activation of TGF-β/Smad3-IL-6 and NF-κB pathways and leads to synovial inflammation in RA patients and collagen-induced arthritis (CIA), which is associated with the imbalance in TH17/Treg response by a 2.8-fold increase in the Th17/Treg ratio (9). The gene discussed is SMAD3; the disease is rheumatoid arthritis.