In this study, the pharmacological stimulation of A3AR, via Cl-IB-MECA, decreased TNF and IL-1β production and attenuated NF-κB p65 activation in colonic tissues in patients with ulcerative colitis, thus corroborating the use of A3AR agonists as an efficacious treatment for IBD patients [11]. The gene discussed is TNF; the disease is ulcerative colitis.