Although the precise mechanism of action underlying development of CAC remains incompletely understood, pro-inflammatory cytokines and mediators produced during chronic inflammation in IBD are thought to implicated in CAC through their capacity to activate Janus kinases 2 (Jak2), and signal transducer and activator of transcription 3 (Stat3), thereby contributing to development of neoplastic cells transformed from colonic epithelial cells [6,7]. Here, STAT3 is linked to inflammatory bowel disease.