EGFR and glioblastoma: Lastly, we have reported that IPA treatment inhibited mitochondrial respiration in U87MG cells and the same cells engineered to over‐express EGFR wild‐type (U87MG‐EGFRwt) or EGFRvIII (U87MG‐EGFR‐vIII), as well as in primary GBM patients‐derived cells, by preventing the translocation of EGFR/EGFRvIII on the mitochondria through the inhibition of Y845 phosphorylation of EGFR [24].