Later work using a mouse model of arthritis induced by albumin plus IL-1β in NFAT5-haploinsufficient mice showed that NFAT5 and the NFAT5-induced chemokine CCL2 were positive contributors to the inflammatory pathology of RA in the arthritic lesion, also finding that CCL2 was a macrophage prosurvival factor (74). This evidence concerns the gene CCL2 and arthritic joint disease.