To examine whether the tumor-suppressive role of PIP4K2A is dependent on its kinase activity, we generated and integrated inactive mutants PIP4K2AN251S (Fedorenko et al., 2008) and PIP4K2AG131L/Y138F into GBM cells and assessed their inhibition effects on AKT phosphorylation and short-term proliferative kinetics. This evidence concerns the gene AKT1 and neoplasm.