However, closer analysis of the data reveals more subtle methylation changes in these pathways (potential silencing of arthritis-promoting JAK1, STAT3, STAT5b and PIAS3 elements and activation of -antagonistic STAT6 and PIAS1) that are consistent with the observed functional SF phenotypes [79,80], although the significance and robustness of these data await confirmation by higher power analysis of the treatment groups in terms of individual mice. This evidence concerns the gene STAT6 and arthritic joint disease.