Further, CRC patients were found to have significantly higher abundance of genes coding for virulence factors, such as FadA, colibactin, and bile acid-inducible operon from some Clostridium spp., though no change was noted for B. fragilis toxin.31 In mouse models of CRC, administering the gut microbial metabolite gallic acid, even when the gut microbiome was not intact, was able to cause a malignant phenotype when a mutation in tumor suppressor p53 was present.32 The gene discussed is TP53; the disease is colorectal carcinoma.