This phenotype is frequently induced by hypoxia, which, through activation of the hypoxia-induced factor 1α (HIF-1α)/IL-1β pathway, increases the activity of pathways such as nuclear factor κB (NF-κB) and signal transducers and activators of transcription 3 (STAT3)—key regulators of inflammatory signaling and glioma cell survival [3,4,5,6]. This evidence concerns the gene STAT3 and central nervous system cancer.