It is tempting to suggest that EGFR activation could relieve the scaffold-mediated inhibition exerted by GRK2 on CXCR4/ACKR3 signaling, by sequestering the protein away these receptors and/or via tyrosine phosphorylation mechanisms, overall switching GRK2 towards its ERK1/2 stimulation mode reported in other BC cell lines [25], leading to a stronger activation of this pathway. This evidence concerns the gene CXCR4 and breast cancer.