The production of autoantibodies (antinuclear antigen, anti-dsDNA and antiphospholipid) during treatment is well documented and there are several mechanisms proposed [2,3], which include the following: 1) TNF-alpha inhibition that causes B-cell activation and autoantibody production through the upregulation of interleukin-10 [3,4]; 2) an increase in Th2 activity [5], and 3) an increase in bacterial infections [6] that leads to the production of antibodies through molecular mimicry. The gene discussed is IL10; the disease is bacterial infectious disease.