In this case, it may be important to consider that IL-10 is self-regulating, in that it normally feeds back to shut down both its own release and that of TNF-α [82]; but, with the IL-10 deficiency of asthma, there would be no brake on TNF-α, which has its own important proinflammatory and pro-AHR effects [85], which could drive EIA. The gene discussed is IL10; the disease is asthma.