In addition, CAFs induce immunosuppression by expressing immune checkpoints, including CD73, programmed death‐ligand 1 (PD‐L1), PD‐L2, and Fas ligand, which suppress CD4+ and CD8+ T cells in the TME.[72, 73, 74] Here, we revealed that a transmembrane hydrolase expressed by a subset of CAFs sustains tumor stemness by degrading an antitumor peptide. The gene discussed is CD4; the disease is neoplasm.