To explore this possibility in GBM, we examined whether a sustained pharmacological blockade of Nav and its subsequent downregulation may result in an increase of the extracellular signal-regulated kinase (ERK1/2) and PI3K/Akt/mTOR cascade, two signaling pathways notably implicated in promoting cell cycle progression and differentiation in cancer cells [55, 56]. The gene discussed is AKT1; the disease is glioblastoma.