Responses to conventional drug therapy differacross IMIDs. Probably the best example is nonsteroidalantiinflammatory drugs, which workin axial spondyloarthritis and psoriatic arthritisbut are less effective in rheumatoid arthritis; inCrohn’s disease and ulcerative colitis, they canhave adverse effects due to impairment of epithelialbarrier function. Furthermore, conventionalimmune modulatory agents show predilectionsfor efficacy in individual IMIDs, with methotrexateused in rheumatoid arthritis, sulfasalazine inpsoriatic arthritis and spondyloarthritis (thoughmostly in peripheral, not axial, disease), azathioprinein IBD, and cyclosporine in ulcerativecolitis (Table 1). Nonetheless, it has been notoriouslydifficult to link these drugs to single cytokineexpression patterns, since their mode ofaction is based on inhibiting several differentinflammatory pathways and is not truly pathogenesis-driven in inception. Furthermore, the subgroupof patients who have an excellent responseto conventional drugs is limited, which suggeststhat master control pathways in individual diseasesare not targeted.