Previous studies have found that transgenic mice with hepatic overexpression of APOC3 are more likely to develop nonalcoholic steatohepatitis and hepatic insulin resistance.[39] Recent studies have shown that APOC3 is involved in regulating inflammatory responses and tissue damage, and silencing APOC3 can alleviate lipopolysaccharide-induced acute lung injury by inhibiting toll-like receptor signaling pathways.[40] The liver is an important site of lipid protein metabolism and APOC3 synthesis. Here, APOC3 is linked to metabolic dysfunction-associated steatohepatitis.