Subsequent comprehensive studies involving larger numbers of well-classified medulloblastoma samples have significantly extended these genetic findings and further confirmed that dysregulation of the KMT2D/KMT2C pathway, including mutations in a KMT2D- and KMT2C-associated demethylase KDM6A, plays an important role in driving various types of human medulloblastomas [14-17]. This evidence concerns the gene KMT2D and medulloblastoma.