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). This evidence concerns the gene MAPT and glioblastoma.