Cytokines are believed to be crucial mediators of chronic intestinal 
inflammation in inflammatory bowel diseases (IBD) such as Crohn's disease (CD) 
and ulcerative colitis (UC). Many of these cytokines trigger cellular effects 
and functions through signaling via janus kinase (JAK) and signal transducer and 
activator of transcription (STAT) molecules. In this way, JAK/STAT signaling 
controls important events like cell differentiation, secretion of cytokines or 
proliferation and apoptosis in IBD in both adaptive and innate immune cells. 
Moreover, JAK/STAT signaling, especially via the IL-6/STAT3 axis, is believed to 
be involved in the transition of inflammatory lesions to tumors leading to 
colitis-associated cancer (CAC). In this review, we will introduce the main 
cellular players and cytokines that contribute to pathogenesis of IBD by 
JAK/STAT signaling, and will highlight the integrative function that JAK/STATs 
exert in this context as well as their divergent role in different cells and 
processes. Moreover, we will explain current concepts of the implication of 
JAK/STAT signaling in CAC and finally discuss present and future therapies for 
IBD that interfere with JAK/STAT signaling.