AKT1 and Alzheimer disease: Evidently, the AKT paradox adds a major qualification to the model presented in Figure 3B; which we presented as is for the following two reasons: (1) decreased GLUT transporter expression, decreased synaptic integrity, and increased GSK3β activity have been more consistently observed in the AD brain (Leroy et al., 2007; Liu et al., 2008; Llorens-Martín et al., 2014; Wan et al., 2014) and (2) pharmacological activators of AKT have demonstrated therapeutic efficacy in Drosophila and mouse models of AD (Zhang et al., 2016; Yi et al., 2018), whereas the same cannot be said for AKT inhibitors.