In a mouse model of colitis, melatonin inhibited the increase of IL-1β, IL-17 and TNF-α, whereas in TLR4 knockout mice melatonin has been found to fail to inhibit effectively the increased levels of IL-1β, IL-17, and TNF-α (Kim et al., 2020), suggesting that melatonin may suppress the LPS/TLR4 signaling pathway by inhibiting expression of pro-inflammation cytokines. The gene discussed is TNF; the disease is colitis.