TNF and arthritic joint disease: A previous study showing that solnatide activates ENaC in mice lacking both TNF receptors (37) and the recent demonstration that depletion of the α subunit of the ENaC blunted the protective effect of solnatide in a TNF-induced inflammation in glomerular endothelial cells (19) led us to propose that there is a high likelihood that solnatide exerts its anti-inflammatory effects in mBSA arthritis via a mechanism independent of the classical TNF receptors but dependent upon the interaction between the lectin-like domain of the cytokine mimicked by solnatide and ENaC.