We hereby describe how the anti-α4β7 drug modulates the DC migratory capacity towards CCL2 in IBD and HCs, thereby expanding our current knowledge on the mechanisms of action of biological drugs, as well as on the surface markers implicated in the recruitment of circulating immune cells by the GI mucosa, thereby unveiling future targets for new treatments for IBD. The gene discussed is CCL2; the disease is inflammatory bowel disease.