The role of gut-derived acetate was further studied in a MASLD-HCC mouse model, in which Bifidobacterium pseudolongum was markedly depleted, and its metabolite, acetate, was found to exert protective effects by restoring gut barrier integrity, suppressing LPS translocation, and inhibiting the pro-oncogenic IL-6/JAK1/STAT3 pathway via GPR43 signaling in hepatocytes, ultimately reducing tumor burden [71]. This evidence concerns the gene STAT3 and neoplasm.