APC and medulloblastoma: Familial disease/germline mutations describe a notable proportion of medulloblastomas (5–10%); predominantly Gorlin (PTCH1/SUFU mutation in SHH patients), Turcot (Adenomatous-polyposis-coli (APC) in WNT patients), Li-Fraumeni (TP53 in SHH patients) and Fanconi’s Anaemia (BRCA2/PALB2, subgroup unknown); they are associated with systemic radio- and chemosensitivity and must also be considered in therapy selection [30].