Protein kinases are fundamental components of diverse signaling pathways, including immune cells, making them effective therapeutic targets in IMIDs. Many cytokines are key regulators of IMIDs that utilize the Janus kinase (JAK) and signal transducer and activator of transcription (STAT) pathway to wield their effect. JAK inhibition blocks the actions of type I/II cytokines, and thus has spurred the development of JAK-inhibitors for the treatment of rheumatoid arthritis (RA) and other inflammatory diseases. Autoimmune-related JAK-inhibitors were first approved for use in RA, followed by ulcerative colitis, and are now being explored in other IMIDs including psoriasis, and atopic dermatitis. This session will focus on the underlying inflammatory targets and the role of the JAK/STAT pathway across immune-mediated conditions as a rationale for the development of JAK inhibitors. The most recent data surrounding current and emerging JAK-inhibitors across IMIDs will be presented and a discussion on how these agents may best fit within evidence-based treatment plans will be explored.