In vivo studies using an animal model of rheumatoid arthritis showed that genistein inhibited IFN-γ secretion and simultaneously enhanced interleukin 4 (IL-4) production by peripheral blood mononuclear cells (PBMCs), which contributed to maintaining a balance between T helper type 1 (Th1) and 2 (Th2) responses23,24. The gene discussed is IL4; the disease is rheumatoid arthritis.