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These networks revealed several previously unrecognized aspects of UC pathogenesis. These included the identification of a cytokine subnetwork that is unique to treatment-naive patients with UC, of cytokines with altered interaction patterns across UC disease states (including IL-22, TL1A, IL-23A, and OSM), and of cytokine-cytokine interactions that were mediated by specific members of the Janus-associated kinase (JAK) family. In particular, our network analysis positioned TL1A as an important upstream regulator of TNF and IL-23A (both of which are targeted by approved UC drugs) and suggested it as a potential therapeutic target. 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