Previous works had shown that MTX inhibited NF-κB activation by increasing both adenosine release and the activation of the adenosine receptor A2a in rheumatoid arthritis [31] and that MTX decreased the TNF-α-mediated activation of NF-κB in Jurkat through the inhibition of IκBα phosphorylation and degradation [3], as well as by releasing adenosine, although the dose (10 μM) and length of treatment (60 min) varied significantly from our experimental conditions. This evidence concerns the gene TNF and rheumatoid arthritis.