Constitutive activity of the RAC-α serine/threonine-protein kinase (AKT) is a common feature of highly invasive gliomas that can be caused by amplification of receptor tyrosine kinases, activating mutations in phosphoinositide 3-kinase (PI3 K) subunits or functional inactivation of the tumor suppressor protein phosphatase and tensin homolog (PTEN) [11]. Here, ERN1 is linked to glioma.