This is in line with earlier observations in an in vivo mouse model showing that compensatory homing via the α4β1/vascular cell adhesion molecule (VCAM)-1 pathway might bypass α4β7 blockade in CD (23) and matching to rodent data that propose considerable redundancy in different homing pathways (25, 26) and VCAM-1-dependent homing as an important pathway in CD-like experimental colitis (27). This evidence concerns the gene VCAM1 and colitis.