Others [24] have suggested that IKKβ is important in this response and that IKK promotes Rictor association with mTOR in the mTORC2 complex, but our data (at least in the cancer cells studied) indicate that IKKα is more important than IKKβ in controlling Akt activation and that there is no reduction in Rictor-mTOR association following IKKα knockdown. The gene discussed is AKT1; the disease is cancer.