In addition, under low sugar conditions, GDH1 is phosphorylated at serine 384 and interacts with RelA and IKKβ, and α-KG directly binds and activates IKKβ and NF-κB signaling, which promotes glucose uptake and tumor cell survival by upregulating glucose transporter 1 (GLUT1), thereby accelerating the formation of GBM [114]. This evidence concerns the gene IKBKB and neoplasm.