Given the role lymphotoxin, TNF-α, and Th cells may play in inflammation and RA pathogenesis, and the additional role soluble LTα3 may play in disease pathogenesis [10-15], we generated a fully humanized blocking and depleting anti-LTα monoclonal antibody (MLTA3698A, pateclizumab) that blocks LTα3-TNFR interactions, LTα1β2-LTβR interactions, specifically depletes LTα1β2-expressing lymphocytes [4]. This evidence concerns the gene TNFRSF1A and rheumatoid arthritis.