AKT1 and glioblastoma: Altogether, these findings showed for the first time that Tau is an upstream regulator of the PI3K/AKT signaling, likely through the remodeling of microtubules favoring the correct delivery of N-cadherin into the membrane; hence, the AKT activity is necessary for Tau-dependent cell migration during the EMT, while the upstream PI3K activity is rather involved in the control of growth and survival of GBM cell tumors (see also Figure 3).