Finally, it will be important to validate the role of PKM2 in regulating Cdk1-cyclinB activation in other tumor types and to define in more detail how PKM2 binding contributes to Cdk1 activation, and perhaps more importantly, to determine if molecules can be developed that alter the interaction and can be used therapeutically to disrupt the elegant linkage between metabolism and cell cycle regulation necessary for tumor cell growth. Here, CDK1 is linked to neoplasm.