This is important not only because this chemokine is upregulated in human IBD, with increased CCL2 levels having been reported in the mucosa of IBD patients as determined by immunohistochemistry and ELISA [20] but also, because mice with either this chemokine genetically deleted [21], or with its receptor (CCR2) deleted [22] are protected from developing experimental colitis. This evidence concerns the gene CCL2 and inflammatory bowel disease.