GBM develops through genetic mutations, including those involved in cell cycle arrest, such as p53, RTK/RAS/PI3K, retinoblastoma (RB), and isocitrate dehydrogenase (IDH1) that promote uncontrolled GBM cell proliferation.15,16 Other mutations promote the remodeling of their microenvironment, co-opting the neighboring neurons, glial cells, cancer-associated fibroblasts (CAF), endothelial cells, and immune cells. This evidence concerns the gene IDH1 and glioblastoma.