Moreover, mRNA and protein expression of ApoA5 was remarkably increased in mice with HFD-induced NASH (Ress et al., 2011; Feng et al., 2015; Lin et al., 2017), implying that the inhibitory effects of ApoA5 on TLR4-mediated signaling pathway depended on the reduction of circulating LPS concentrations in mice with HFD-induced NASH. Here, APOA5 is linked to metabolic dysfunction-associated steatohepatitis.