In vitro and in vivo studies showed that human LF (hLF) was able to suppress tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-1 expression by mononuclear cells in response to lipopolysaccharides (LPS) and could regulate inflammatory processes [67], such as colitis amelioration in rats, by enhancing IL-4 and IL-10 cytokine production [68]. The gene discussed is TNF; the disease is colitis.