We acknowledge that GRK3 in breast cancer is unlikely to be affecting CXCL12/CXCR4 interactions exclusively in vivo and could certainly be affecting additional chemokine receptors such as CXCR7 [50–52], CXCR3 [53, 54], CCR7 [55–57], and others.[58] However, our data support a strong role for GRK3-mediated regulation of CXCL12 metastatic responses, arrestin-mediated recruitment, and CXCR4 receptor internalization in vitro (Figs 3, 4 and 7). Here, SAG is linked to breast carcinoma.