Interestingly, the effect of Gβγ inhibition on cell growth can be mimicked by a specific Gβγ inhibitor, gallein, or pertussis toxin treatment, indicating that the Gβγ is predominantly liberated from activated Gi/o proteins that couple to many GPCRs overexpressed in prostate cancer cells, such as CXCR4 and LPA receptors [13, 32, 36]. This evidence concerns the gene CXCR4 and prostate carcinoma.