Butyrate is capable of inhibiting colorectal cancer (CRC) proliferation through various mechanisms, such as the induction of autophagy-mediated β-catenin degradation (Garavaglia et al., 2022), the upregulation of TLR4 expression, and the activation of the MAPK and NF-κB pathways (Xiao et al., 2018), The antiproliferative effect of acetate may be attributed to its influence on mitochondrial metabolism; acetate has been shown to reduce the proliferation of tumor cell lines HT29 and HCT116 and to decrease glycolysis under normoxic conditions (Sahuri-Arisoylu et al., 2021). This evidence concerns the gene TLR4 and colorectal carcinoma.