We previously showed a loss of kinin moiety on the surface of synovial neutrophils of rheumatoid arthritis patients, resulting in lower neutrophil expression of TK and PK, while synovial levels of kallikreins are elevated showing that kallikreins are actively involved in the generation of kinins by circulating and synovial neutrophils, to promote synovial tissue remodelling and to sustain joint inflammation [8]. This evidence concerns the gene TKT and rheumatoid arthritis.