Strikingly, the levels of autophosphorylation of PDK1 at the Ser241 activation loop site, and those of Akt at both Thr308 and Ser473 activating residues were 50% higher both in the cortex (Figure 2A) and the hippocampus (Figure 2B) of the 3xTg-AD transgenic mice, which was accompanied by similar increase in the phosphorylation of the Akt substrate PRAS40 at Thr246 and, to a lesser extent, of GSK3β at Ser9 and FOXO1 at Ser256, their specific Akt sites. The gene discussed is FOXO1; the disease is Alzheimer disease.