Since it has recently been reported that epithelial malignancies of the adult gut are induced by both chronic inflammation and abnormal SHH expression or signaling, and that inflammatory environments often increase the expression of SHH ligands [28, 29], the SHH signaling–related transcription factor Gli-1 is a central mediator of the IL-6 signaling network and thereby can initiate the tumor microenvironment in CAC and regulate the progression of precursor lesions and tumor formation. This evidence concerns the gene SHH and neoplasm.