CFB and arthritic joint disease: In in vivo studies, CP-25 exerts its therapeutic effects in experimental arthritis by directly targeting GRK2 through multiple mechanisms (1): enhancing GRK2 protein stability while suppressing its enzymatic activity via inhibiting EP4 receptor translocation (48); (2) disrupting GRK2-Gβγ interactions to restore EP4 receptor responsiveness (53); (3) blocking Ahr activation and its association with GRK2 (49); (4) attenuating CXCR4/Gβγ/PI3K/AKT signaling through GRK2 translocation blockade (54).