Because it was shown that PLADs preferentially undergo homotypic interactions, i.e., a TNFR1-sPLAD binds preferentially to a membrane expressed TNFR1, the strong therapeutic effect of TNFR1-sPLAD validates TNFR1 as a therapeutic target for arthritis and potentially other inflammatory diseases as well. This evidence concerns the gene TNFRSF1A and arthritic joint disease.