Preclinical studies have shown that MC38 models in CAF-rich mice have difficulty benefiting from tumor vaccines and anti-PD-1 therapy, possibly because CAFs exclude CD8+ T cells (not CD4+ T cells) from tumors by producing NOX4 T cells (or macrophages) to inhibit the response extensively, and pharmacological inhibition of NOX4 restores the immunotherapeutic response of CAF-rich tumors [306]. Here, CD8A is linked to neoplasm.