In addition, jun is an essential mediator of TLR-induced inflammation and a critical target of Jun N-terminal kinase (JNK) in mediating activation of the p53 signaling pathway.21, 22 The TLR signaling pathway is associated with the production of pro-inflammatory cytokines and activation of innate immunity and might also activate Jun N-terminal kinase and NF-κB signaling in the development of NAFLD.23, 24 In our experiments, increases in jun, ccl3 and cxcl10 in the TLR-mediated signaling pathway provided supporting evidence for this hypothesis. Here, CCL3 is linked to metabolic dysfunction-associated steatotic liver disease.