Over the last 10 years, there have been enormous strides in understanding the molecular mechanisms of glioblastoma pathogenesis and much of the work has led to an understanding of how molecular subgroups of glioblastoma patients respond to treatment and their eventual outcome.7 So far the results of these efforts have identified a few key molecular alterations in gliomas such as IDH1,2 mutations as a positive prognostic factor of overall survival, 1p19q codeletion as a hallmark of oligodendrogliomas, and MGMT promoter methylation as a marker of resistance to temozolomide treatment. The gene discussed is MGMT; the disease is glioblastoma.