Further, these cytokines enhanced uptake of exogenous CXCL12, which was inhibited in a dose-dependent manner by antagonism of CXCR7, suggesting that under inflammatory conditions, CXCR7 facilitates internalization of CXCL12, leading to loss of polarity at the BBB seen in EAE as well as MS (Cruz-Orengo et al., 2011). This evidence concerns the gene ACKR3 and myeloid sarcoma.