Despite the involvement of Ras pathway in epithelio-mesenchymal transition via SNAI2 [52] and its link with worse outcome of pediatric HGG [53], we did not find a correlation between H-RAS gain/amplification and its gene expression, nor activating mutations in the RAS genes including BRAF V600E already described in some pediatric supratentorial gliomas [27], again highlighting differential oncogenic mechanisms in DIPG compared to other pediatric HGG. The gene discussed is SNAI2; the disease is diffuse intrinsic pontine glioma.