It protected against NAFLD-HCC by secreting the antitumor metabolite acetate, which reached the liver via the portal vein and inhibited the interleukin 6 (IL-6)/Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway [27]. This evidence concerns the gene STAT3 and metabolic dysfunction-associated steatotic liver disease.