Targeted inhibition of TNF-α/IL-6 signaling may represent a novel therapeutic strategy for retarding RA progression.[21] Jing et al reported significantly elevated serum levels of IL-6 and TNF-α in patients with AS, which were strongly correlated with disease activity (Bath Ankylosing Spondylitis Disease Activity Index), inflammatory markers (CRP, ESR), and imaging grading of sacroiliac joints. This evidence concerns the gene TNF and rheumatoid arthritis.