Under normal conditions, COX-2 expression is low or absent at basal levels but is rapidly induced by several stimuli, and, unlike the constitutive isoform COX-1, COX-2 is frequently overexpressed in cancerous tissues, including glioma and is implicated in cell proliferation, migration, metastatic process, angiogenesis, as well as in cancer stem-like phenotype promotion [11, 12]. This evidence concerns the gene PTGS2 and glioma.