Transposable elements (TEs) are stretches of DNA that are competent to replicate within a genome. In plants, these mobile elements have been extraordinarily successful at doing this, so successful that average stretch of plant DNA in the average plant genome is almost certainly a TE. Because each new insertion can potentially disrupt normal gene function, TE activity can be dangerous. Because of this, plants, like all eukaryotes, have evolved sophisticated mechanisms for repression of TE activity. These mechanisms use small RNAs and chromatin modification to trigger and maintain epigenetic silencing of TEs. Related systems are required for a variety other processes, such as microRNA-mediated down-regulation of genes, resistance to viral infection and imprinting. Although these pathways are often seen as distinct, all of them appear to have at least some role in TE regulation. Indeed we have shown that silencing of one otherwise active TE can involve nearly every known silencing pathway. This means that transposon silencing can serve as an excellent model for understanding epigenetic silencing in general. Our work also suggests that TE silencing can be exquisitely sensitive to developmental cues, particularly distinctions between germinal and somatic lineages, and that TEs can host genes can be coordinately regulated. Future work will involve genome-wide analysis of the impact of TE silencing on host gene function by experimentally inducing epigenetic silencing at a wide variety of loci and comparing those effects with the effects of extant epigenetic variation in maize and related species. Ultimately, the goal is to determine the extent to which TEs have contributed to selectively meaningful genetic and epigenetic variation in plants.