Based on our earlier study demonstrating ILK as a pro-inflammatory molecule (29), we investigated the role myeloid-specific ILK in a mouse model of colitis using myeloid-ILK deficient (M-ILK KO) mice., In this model the pathology of experimental colitis was significantly reduced by myeloid ILK deficiency with the pro-inflammatory signalling during intestinal inflammation dependent on myeloid-ILK (30). This evidence concerns the gene ILK and colitis.