This suggests that the prolonged extrusion of K + from Ab-treated Tg2576 neurons was the cause of apoptosis in this study. This was confirmed by undertaking the same experiments in the presence of the K+ channel blocker 4-AP, which provided significant protection against Ab-induced toxicity in Tg2576 neurons. A novel element to the MIFE approach in this application is that it allows measurement of total flux of K + into- or out- of cells, rather than the flow of K+ through particular channels/ transporters that is observed through patch-clamp recording and pharmacological inhibitor studies. Glioblastoma is a highly aggressive brain cancer that has been designated as grade IV, according to the World Health Organization. It represents an extremely invasive form of glioma and has the worst prognosis of any central nervous system disease. Despite aggressive therapies that include combinations of surgery, radiotherapy and chemotherapy, the median postdiagnostic survival period is approximately one year. Many aspects of glioblastoma contribute to its poor prognosis, including the invasive nature of these abnormal cells and the extreme heterogeneity of this cancer. The lack of specificity for the current treatments and their side effects imply the need to develop new therapeutic strategies that target tumor cells. Microtubule-targeting agents represent an important class of drugs used in the treatment of cancers. Microtubules are ubiquitous cellular polymers composed of heterodimers of a- and b-tubulin subunits. They play major roles in several cellular functions, including intracellular transport, maintenance of cell architecture, cell signaling and mitosis. MTAs exert their antitumoral activity by altering microtubule polymerization and dynamics, which causes growth arrest in mitosis and subsequent cell death by apoptosis. Proteins that compose the intermediate filaments are able to bind free unpolymerized tubulin onto specific sites named tubulin-binding sites and thus can affect microtubule polymerization in vitro and in vivo. A peptide derived from the light QX 314 bromide neurofilament subunit that corresponds to the sequence of TBS can enter specifically into glioblastoma cells by endocytosis, where it disrupts the microtubule network and induces cell death by apoptosis. Recent Radicicol studies have confirmed that interactions between intermediate filaments, notably NFL or Vimentin, and key molecules responsible for the plasticity of the mitochondrial network, including Mitofusin-1 and -2 or Dynamin, are necessary to maintain organelle integrity and to allow mitochondrial motility.