GRK3 and neoplasm: Since 66cl4-luc cells are weakly invasive and this phenotype is unaltered by GRK3 gene silencing (Fig 7B), we propose that the observation of increased metastases of GRK3-deficient 66cl4-luc cells is due to increased migration (Fig 7A), possibly within the tumor microenvironment, leading to higher rates of intravasation that are controlled by other mechanisms.