In order to define the cellular pathways deregulated in gliomagenesis in a Bmi1-dependent, H3K27me3-mediated manner, we used a well-established mouse model of gliomagenesis that relies on the loss of PTEN and p53, two of the most common genetic alterations in IDH wild-type glioblastoma (GBM) [23]. The gene discussed is BMI1; the disease is glioblastoma.