IL1A and rheumatoid arthritis: However, it is unclear whether this is due to biological superiority of TNF-α over IL-1 in RA pathogenesis [4] or whether the approach to block the IL-1 receptor with anakinra is only partly effective in neutralizing IL-1 activity in vivo because of short half-life or inability to achieve sufficient exposure at the target site with the current dosing regimen [5].