In human PBMC-derived, M-CSF, and LPS-treated macrophages, CCL2 secretion is regulated via NFAT5, which is in turn regulated by proinflammatory M1 polarizing and hypoxic stimuli, and confers apoptotic resistance to human RA macrophages and murine peritoneal and splenic macrophages. This evidence concerns the gene NFAT5 and rheumatoid arthritis.