Our integrative analysis found the expected distributions of clinical, pathological, and molecular features within WHO-defined medulloblastoma entities and their provisional sub-variants1 in the HIT-SIOP PNET 4 cohort (CTNNB1 mutation and chromosome 6 monosomy in WNT medulloblastoma; desmoplastic/nodular pathology and TP53 mutation in SHH medulloblastoma; i17q in non-WNT/non-SHH-medulloblastoma; and SNCAIP duplication and MYCN amplification in Group4; figure 1). Here, SNCAIP is linked to medulloblastoma.