Based on this theoretical basis, Wan et al. demonstrated that transplantation of healthy human feces via FMT into a rat model of CCL4-induced liver failure reduced inflammatory response mediators such as TLR4 and TLR9 and circulating pro-inflammatory factors such as IL-1β, IL-6, and TNF-α It also helped restore tight junction proteins in the intestinal mucosal barrier, reduced blood ammonia levels, ameliorated liver necrosis, and improved behavior and spatial learning ability in the animal model, ultimately preventing the occurrence of HE (Wang W. W. et al., 2017). The gene discussed is TNF; the disease is liver failure.