Simultaneously activating the autophagy pathway, but independently of the ALPK1/TIFA signaling.112 F. nucleatum treatment not only modulates metabolite levels but also regulates gut microbiota dysbiosis, notably reducing butyrate-producing bacteria, thereby hindering butyric acid synthesis.113 It also enriched pathogens linked to CRC development, including intestinal oncogenes, PPAR signaling pathway of cyclic adenosine monophosphate, and recruited eight taxonomic groups of Proteobacteria to change mucosal microflora.114. The gene discussed is ALPK1; the disease is colorectal carcinoma.