DNA methylation or 5-methylcytosine (5mC) is crucial for embryonic development and plays important roles in the control of gene expression, genome stability and silencing of transposable elements. It was recently shown that the TET family of enzymes can oxidize 5mC to 5-hydroxymethylcytosine (5hmC) as part of a potential demethylation pathway. We and others have shown that TET1 and 5hmC help to maintain the pluripotency network in mouse embryonic stem (ES) cells by preventing methylation of pluripotency-associated genes. We also found that LINE1 retrotransposons are enriched for 5hmC at their 5′ end in ES cells and more recently confirmed this using a quantitative technique for single-base mapping of 5hmC. TET targeting to LINE1 elements maintains them in a hypomethylated state and consequently transcriptionally active. TET enzymes may therefore be involved in controlling retrotransposon mobility and thus implicated on the impact that these potentially mutagenic elements have on the genome. We are currently investigating the role of these epigenetic mechanisms in controlling LINE-1 mobility in ES cells, neural stem cells and during ageing, where increased retrotransposon mobility may contribute to the etiology of neurodegenerative diseases.