The partially different mechanism of TNF-α inhibition between ETN and anti-TNF-α monoclonal antibodies may explain the lesser generation of autoantibodies in patients treated with ETN in comparison with IFX, as well as the clinical efficacy of IFX and ADA but not of ETN in the treatment of granulomatous diseases such as Crohn disease and Wegener granulomatosis. The gene discussed is ADA; the disease is Crohn disease.