It is currently believed that the inflammatory injury of NASH is likely attributed to TLR4 activation by pathogenic (e.g. LPS) and/or non‐pathogenic ligands (e.g. FFAs), triggering recruitment of adaptor protein myeloid differentiation factor 88 (MyD88), which leads to activation of signalling cascades (i.e. NF‐κB and MAPKs) for generation of pro‐inflammatory molecules. Here, TLR4 is linked to metabolic dysfunction-associated steatohepatitis.