Our work in the K/BxN mouse model of RA recently showed that over-expression of the human PON1 transgene, which causes a twofold to threefold increase in circulating PON1 activity, reduces RA joint disease activity and associated with lower levels of the pro-inflammatory oxylipins 5-HETE and 15-HETE [26]. This evidence concerns the gene PON1 and arthropathy.