The fact that similar observations were not so frequent was due to three factors: (1) lack of substantial long-term survivors; (2) the patients having RA had a more pronounced immunodepressed status due to the exposition to several immune modulators, such as corticotherapy, methotrexate, or anti-Tumor Necrosis Factor (TNF) for example; and (3) relative limited efficacy of rituximab in depleting memory B-cells and plasma cell compartment within lymphoid organs [16]. The gene discussed is TNF; the disease is rheumatoid arthritis.