While our study places CAMKKβ upstream of AMPK to induce Akt activation under EGF treatment, we cannot rule out the possibility that CAMKKβ may directly induce Akt activation under EGF treatment, since a recent report showing that CaMKKβ could directly phosphorylate Akt at T308 in a Ca2+/CaMKKβ dependent manner in ovarian cancer cells43. This evidence concerns the gene PRKAA1 and ovarian cancer.