An upregulation of ZNF395 after hypoxia was described for additional glioblastoma-derived cell lines [8, 9] and most importantly an increased expression of ZNF395 as a part of a hypoxic response was observed in human solid tumors such as GBMs [8] and neuroblastomas [13] implying that also in these in vivo situations ZNF395 enhances the hypoxic induction of these proinflammatory factors and may thus significantly contribute to disease progression. This evidence concerns the gene ZNF395 and glioblastoma.