Considering that α-tubulin was downregulated in AD-like conditions [Fig. 2B(i),C], we checked the activity of Gsk3β, a kinase that hyperphosphorylates tau, leading to destabilization of the microtubule network, and found that its activity was increased significantly 1.17-fold under condition A but decreased significantly 1.46-fold under condition B [Fig. S4(i),(iii)], whereas the activity of its upstream effector AKT was decreased significantly 2.44-fold under condition A [Fig. S4(i),(ii)]. The gene discussed is AKT1; the disease is Alzheimer disease.