Previous studies of ispinesib resistance by Kenchappa et al.24 also concluded that glioma cells activate anti-apoptotic mechanisms to survive the prolonged G2M block produced by ispinesib, whereas normal cells apoptose under these conditions due to “mitotic catastrophe.” This phenomenon was shown to be mediated by STAT3 through its transcriptional activity and effects on mitochondrial membrane permeability and oxidative metabolism. The gene discussed is STAT3; the disease is central nervous system cancer.