Taken together, these observations suggest that a variety of mechanisms can lead to aberrant NF-κB activation in GSCs, consistent with the above-mentioned demonstration that a plethora of deregulated processes, including EGFR amplification, PTEN deletion, and monoallelic NFKBIA deletion, have been associated with deregulated NF-κB activation in GBM. This evidence concerns the gene PTEN and glioblastoma.