Since the PDK1 L155E mutation abrogating PDK1 signaling with intact Akt activation caused profound alterations in mice (Cordón-Barris et al., 2016), we postulated that inhibition of Akt might have protected mice against AD, whereas inhibition of the docking-site dependent PDK1 substrates might have been responsible for the toxicity of the treatment. The gene discussed is AKT1; the disease is Alzheimer disease.