Similarly, CCL8 promotes immunosuppression in the tumor microenvironment by recruiting myeloid-derived suppressor cells,[45] and in intestinal inflammation, CCL8 is linked to visceral pain severity.[46] This functional switch may depend on gut-specific microbiota-metabolite microenvironments; for example, SCFAs downregulate proinflammatory CCL8 isoform expression via histone deacetylase inhibition while enhancing the transcription of its anti-inflammatory variants.[47]. The gene discussed is CCL8; the disease is neoplasm.