Despite the identification of key genetic alterations in glioblastoma (GBM), which drive hyperactivation of key cell signaling pathways regulating cell survival and proliferation, such as the PI3K and mitogen activated protein kinase (MAPK) pathways, therapies targeting pathway factors have not led to improved patient outcome1, 2 and postdiagnosis survival for GBM patients is still measured in months. The gene discussed is WNK2; the disease is glioblastoma.