Consistently, depletion of FAP+ fibroblasts using engineered FAP chimeric antigen receptor T cells resulted in reduced tissue damage and ECM deposition in experimental models of angiotensin II/phenylephrine–induced cardiac damage and bleomycin-induced lung fibrosis as well as reduced leukocyte infiltration and disease severity in a murine model of arthritis (49–51). This evidence concerns the gene FAP and Arthritis.