The cascade of these events (tp53 mutation inducing aberrant SA metabolism, followed by pathobiont blooming and inflammation) may be a novel mechanistic explanation for the role of tp53 mutations at early stages of CAC progression [11, 12], and may also be consistent with a metabolic shift to host glycan utilization by the human CRC microbiome during cancer progression [27]. The gene discussed is TP53; the disease is colorectal carcinoma.