For example, FAPα+ fibroblasts impair the responsiveness to the T-cell-activating immune checkpoint inhibitors α-CTLA-4 and α-PD-L1 via the secretion of CXCL12.325 Moreover, the secretion of CCL2 by FAP+ fibroblasts promotes the recruitment of MDSCs,326 indicating the importance of FAP in modulating the deleterious biological behaviors of CAFs.327 However, recent studies have suggested that inhibiting FAP-positive CAFs can induce cancer cachexia. The gene discussed is CTLA4; the disease is cancer.