JAK1 and arthritic joint disease: 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.