As its core mechanism involves targeting of interleukin (IL)-17 responses, which despite being pathogenic in RA are important for combating infection, we discuss how its selective targeting of IL-17 production by T helper type 17 (Th17) and γδ T cells, while leaving that of CD49b+ natural killer (NK and NK T) cells intact, reflects the ability of helminths to modulate the immune system without immunocompromising the host. The gene discussed is IL17A; the disease is infection.