Taking into account the findings by Drury et al. who showed in colon carcinoma cells that monomeric but not dimeric CXCL12 preferentially recruited β-arrestin to CXCR4 (130), one could hypothesize that enhanced β-arrestin signaling through ACKR3 is due to preferential binding of monomeric CXCL12. Here, CXCL12 is linked to colon carcinoma.