This dysbiosis is facilitated by various pathways, including the production of tumor-accelerating and SASP-accelerating metabolites such as DCA derived from the dysbiotic microbiome, the increase in hepatic contact with microbiome-associated molecular patterns (MAMPs) such as LPS and the reduction in the accumulation of CD8+ T cells and NKT cells in the hepatic microenvironment, as well as consistent hepatic exposure to tumor-promoting cytokines such as IL-25. The gene discussed is CD8A; the disease is neoplasm.