Medulloblastoma (MB) is one of the leading types of brain cancer, which is a common and highly malignant type of cancer affecting children. Despite next‑generation sequencing revolutionizing the mutational data in MB, a complete understanding of its causes and epigenetic mechanisms remains to be achieved. Multiple epigenetic mechanisms, including DNA methylation, histone modifications and non‑coding RNAs, have been implicated in MB. Additionally, these mechanisms are interconnected; for example, O6‑methylguanine‑DNA methyltransferase (MGMT) hypermethylation predisposes to mutations in the key tumor suppressor genes, Tp53 and K‑RAS, and MGMT hypermethylation has also been detected in patients with MB. Isocitrate dehydrogenase 1 (NADP+) (IDH1) mutations alter the whole methylation landscape of certain genes, including the differentiation marker, NeuroD1. IDH1‑CIMP has been recognized in sonic hedgehog‑activated MB samples. The 5S rRNA gene is only expressed in the case that histone H4 is acetylated in its nucleosome; without this modification, transcription factor IIIA does not bind to it. Similarly, the GAL4A activator cannot transcribe DNA without acetylated histones. A number of non‑coding RNAs, such as miR‑9, miR‑10, miR‑124, miR125a, miR‑125b and miR‑324‑5p are the driving force behind the growth and differentiation of granular neuronal precursor cells (GNPCs). They protect GNPCs from constant proliferation and trigger differentiation. In the future, the author aims to use epigenetic candidates, such as NeuroD1 and Nestin that activate tumor differentiation and identify more candidates that induce MB differentiation, as a new hope for MB therapies. The present review discusses the epigenetic mechanisms involved in MB proliferation, and whether they can be employed as weapons against the disease.

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