S100A4 and neoplasm: Considered alongside the methylation-dependent transcriptional silencing observed for S100A4 in medulloblastoma cell lines (Figure 2A), these findings support (i) the somatic hypermethylation-associated transcriptional silencing of S100A4 in the normal cerebellum, and (ii) tumour-specific hypomethylation of S100A4 in a subset of medulloblastomas, consistent with elevated expression and a pro-tumourigenic role.