Previous studies have defined a dichotomous role of IEC-specific STAT3 in mediating resistance to DSS-induced epithelial damage, as well as in enhancing tumor growth.52,53 Hence, based on these bioinformatic findings, the impaired STAT3 downstream signaling and context-dependent role of STAT3 in different pathogenic milieu may account for the seemingly contradictory in vivo results. This evidence concerns the gene STAT3 and neoplasm.