They reported that silencing Eag1 reduced the viability and proliferation of the U87MG glioblastoma cell line and increased the apoptotic rate triggered by temozolomide (TMZ) [148], clearly pointing out and confirming a role for potassium channels (Eag1) in modulation apoptosis in a glioma context. This evidence concerns the gene KCNA3 and glioblastoma.