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. The gene discussed is MAPK3; the disease is breast cancer.