During AD, Aβ aggregates worsened mTORC1 signaling due to 40 kDa proline-rich Akt substrate phosphorylation (PRAS40), leading to mTORC1 activity enhancement and autophagy inhibition (Caccamo et al., 2011; Tramutola et al., 2015) (Figure 6). The gene discussed is AKT1; the disease is Alzheimer disease.