Consistently, splenocytes and T lymphocytes isolated from GRK2+/− mice display increased agonist-induced activation of ERK and PI3K/Akt pathway.25 Stable overexpression of GRK2 in breast cancer cells significantly facilitated both mitogenic (ERK1/2) and pro-survival signaling (AKT) in response to heregulin or EGF.26 Our experimental data demonstrated that ablation of eIF3d can significantly decrease GRK2 protein level. This evidence concerns the gene PIK3CG and breast carcinoma.