Metagenomic analysis also suggested that Atg16l1∆IEC mice may have a higher capacity to produce fucosylated oligosaccharides (via GDP-L-fucose synthase), with this function also found in fucose-carrier Bacteroides species of Crohn’s disease patients.89 Metabolomic profiling only revealed a suggestive trend of fecal L-Fucose in Atg16l1∆IEC mice at trimester 3, which may warrant further investigation due to the important role of fucosylation as a post-translational protein modification in Crohn’s disease and colorectal cancer.26,90–92. This evidence concerns the gene GFUS and colorectal cancer.