In an animal model of non-alcoholic steatohepatitis (NASH), various factors such as metabolic disorders, oxidative stress, and translocated bacterial products activated Kupffer cells via TLRs, especially TLR4, leading to increased NF-κB signaling and pro-inflammatory cytokine production [99]. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatohepatitis.