For example, LPS derived from gut microbiota leaks from the gastrointestinal tract to the whole body through disruption of gut homeostasis, and LPS-induced TNF-α damages the liver and induces the development of nonalcoholic steatohepatitis [12], in which IL-17 levels in the intestine are increased, and liver inflammation is promoted by the migration of T-helper (Th) 17 cells from the intestine to the liver and the secretion of IL-17 [13]. Here, IL17A is linked to metabolic dysfunction-associated steatohepatitis.