Although CDK-2 expression in glioma cells is not very high compared with other tumor types according to the Human Protein Atlas (www.proteinatlas.org, Version 22.0), CDK-2 and its cyclin partners play an important role in regulating the G1/S phase transition and are usually abnormally activated in glioma [33, 34], thereby implicating CDK-2 as a target for the design of therapeutic inhibitors for GBM. The gene discussed is CDK2; the disease is neoplasm.