The cohort included SMARCB1-deficient ATRTs that could be unequivocally assigned to the ATRT–SHH molecular group based on DNA methylation-based CNS tumor classification [2], but shows high diversity with regard to patient age, tumor location, tumor volume and histopathological findings, reflecting the high degree of heterogeneity commonly observed in ATRT–SHH. This evidence concerns the gene SMARCB1 and neoplasm.