FAPα, a cell-membrane dipeptidyl peptidase (83), was remarkably higher in synovial tissue along with cultured synovial fibroblasts isolated from individuals who fulfilled classification criteria for RA in contrast with patients in whom joint inflammation resolved, implying that FAPα expression might be linked to a pathogenic fibroblast phenotype (84, 85). The gene discussed is FAP; the disease is rheumatoid arthritis.