Additionally, although enteric glia appear to be activated by intestinal inflammation, selectively knocking out a number of inflammatory response pathways (e.g. STAT3, MYD88, RELA, and IFNGR1) in GFAP+ enteric glia did not affect their pro-tumorigenic function, supporting the view that the role of GFAP+ enteric glia in CRC might be independent of inflammatory mechanisms. This evidence concerns the gene GFAP and colorectal carcinoma.