In mice subjected to the DEN-CCl4 model, reduced gut microbial diversity and lower acetate levels were associated with increased IL-17A-producing group 3 innate lymphoid cells (ILC3s) and greater tumor burdens, whereas restoring acetate through fecal microbiota transplantation or supplementation suppressed IL-17A production via histone deacetylase inhibition and Sox13 downregulation, thereby limiting fibrosis and tumor progression [70]. This evidence concerns the gene SOX13 and neoplasm.