Moreover, gut dysbiosis and gut-derived products stimulate HSCs to express the senescence-associated secretory phenotype (SASP), reprogramming their transcriptome towards the production of inflammatory cytokines, such as IL-1 beta, as observed in mice models of non-fibrotic HCC after the establishment of diet-induced gut dysbiosis [32]. This evidence concerns the gene IL1B and hepatocellular carcinoma.