In the past decades, it has been shown that Il-10 deficient mice with lacking functional Il-10 (Il-10−/−) or Il-10 R2 subunit (Il-10 Rb−/−) developed spontaneous enterocolitis [20, 21] which resulted from unbalanced Th1/Th17 response, excessive release of proinflammatory cytokines (mainly Il-12, Il-13, Il-17, Il-23, IFNγ) and failure in homeostatic relationship between microbiota and the host [16, 17]. The gene discussed is IL10; the disease is enterocolitis.