It has been demonstrated by numerous groups that early cecal pro-inflammatory (disease resistance) signals following initial infection with STm or SE was dramatically downregulated 2–4 days after infection that is linked with the development of an anti-inflammatory, Th2 response (15, 17, 32, 34, 44) to increased expression of IL-10 and TGF-β, which suggests the end of the disease resistance and the start of a disease tolerant state were being initiated. The gene discussed is TGFB1; the disease is infection.