In CRC models, a newer study has shown that by increasing the burden of F. nucleatum in tumors, it can increase the production of butyric acid in tumor cells, thereby inhibiting histone deacetylase 3/8 activity in CD8+ T-cells, promoting TBX21 expression, reducing PD-1 levels, and thus improving CD8+ T-cell function and enhancing anti-PD-1 therapy [157]. The gene discussed is CD8A; the disease is neoplasm.