While these methylation patterns were associated with transcriptional silencing in medulloblastoma cell lines, suggesting that S100A2 is epigenetically silenced by hypermethylation in the normal cerebellum, no clear evidence of aberrant tumour-specific epigenetic regulation in medulloblastoma development was found, and more detailed examination of extended tumour cohorts are now required to further discern any role in medulloblastoma. Here, S100A2 is linked to neoplasm.