“…Moreover, even if high expression of the transgene were successful, the constant high levels of anti-inflammatory molecules might increase the risk of infection, as already observed with anti-TNF-α and anti-IL1 treatment of patients with rheumatoid arthritis (RA). [16][17][18][19] In addition, there might be an adaptive response to the constant high concentration of transgene protein, counteracting its therapeutic effect. Several vectors driven by drug-controlled promoters have been developed to achieve regulated transgene expression; however, this approach requires constant monitoring of the disease to achieve optimal efficacy, and this is further complicated by the unpredictable, relapsing course of the disease.…”