The current consensus is that the predominant effect of CAFs is immunosuppression, collaboration with IL-6, CXC-chemokine ligand 9 (CXCL9), and TGF-β, demonstrating well-established roles in recruiting and activating the myeloid-derived suppressor cells (MDSCs), Treg, and tumor-associated neutrophils and reducing CD8+ T-cell recruitment and responses (4, 5). Nevertheless, the relationship between CAFs and immune cells varies with tumor purity and stromal- or immune-dominant pattern due to spatial heterogeneity in the TME. This evidence concerns the gene CD8A and neoplasm.