Background: CCX-CKR is considered to be a chemokine decoy receptor that is unable to signal. Results: Chemokines induce β-arrestin recruitment to CCX-CKR and pertussis toxin (PTX)-dependent CRE activity. Conclusion: PTX-sensitive G proteins hinder CCX-CKR coupling to other G proteins and consequently keep receptors silent. Significance: Recruitment of β-arrestin to CCX-CKR requests re-evaluation of the signaling capacity of this atypical receptor. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.