Moreover, the interplay between these cofounding alterations has been shown to foster progression to secondary high-grade glioma (sHGG) in pediatric patients, as a comprehensive molecular analysis of a population-based sHGG cohort showed a significant enrichment of MAPK-activating BRAF mutations and a homozygous loss of CDKN2A in these tumors [132,133]. This evidence concerns the gene BRAF and glioma.