implicated several additional histone modifiers in life span determination [6,7]. In addition to the organism’s aging pro� gram, stochastic events can also induce epi� genomic changes over time. For example, human monozygotic twins have very similar DNA methylation patterns at birth, but they also show differences that can increase as they get older [8]. These changes may be attributed to environmental in� uences. Another possi� bility is that unavoidable errors occur during the maintenance of epigenetic patterns due to the disruptive nature of transactions at the genome. Transcription by RNA polymerases has the potential to reshuf�e or even erase epi� genetic signals because it requires the transient eviction and subsequent reassembly of histones in the wake of the polymerase. Indeed, several studies suggest that transcription destabilizes chromatin and leads to the partial eviction of (modified) histones and replacement by newly synthesized (unmodified) ones [9]. It is worth noting however, that the introduction of many of the histone modifications in active regions of the genome is promoted by the process of tran� scription initiation or elongation. Therefore, these marks can be maintained even when the histones carrying the marks are evicted [10]. DNA replication is another potential source of epigenetic rearrangements. Ahead of the replication fork, old modified histones dissoci� ate from the DNA and behind the replication fork, histones reassemble on the two daughter strands. The chromatin gaps on the duplicated DNA are complemented by a set of newly synthesized unmodified histones. In order to maintain an epigenetic identity, the cells need to re�establish the modification pattern of the mother cell by modifying the newly synthe� sized histones in the daughter cells. The speed at which this occurs can substantially differ Epigenetic states help maintain cell identity but they are also dynamic entities that respond to signals. Indeed, cells undergoing developmental changes are characterized by global rearrange� ments of the epigenetic landscape. Recent stud� ies suggest that aging is one such epigenome� shifting developmental event. What is more, epigenetic regulators seem to in�uence the aging process. Aging can occur in different contexts. Here we discuss the emerging evidence that both organismal and cellular aging, as well as histone protein aging, have intimate connections to the epigenome. Striking links between organismal aging and epigenome alterations have recently been identi� fied in humans and metazoan model organisms [1]. For example, tissues and cells of aging organ� isms show increased levels or redistribution of heterochromatic marks such as tri �methylation of lysine 9 on histone H3 (H3K9me3) [2,3]. The cause and biological significance of these changes are still unclear; however, a driver for epigenome changes could be an aging pro� gram that changes the expression of chroma� tin�modifying or �demodifying enzymes. For example, loss of H3K27me3 in (prematurely) aging human brains is accompanied by the increased expression of the H3K27�specific demethylase UTX [4]. Aging somatic cells in Caenorhabditis elegans show a similar decline in H3K27me3 and increase in UTX�1 expression [4,5]. Importantly, genetic inactivation of C. elegans UTX�1 prevents the age�induced loss of H3K27me3 and extends life span of the worm via the insulin�signaling pathway, a major life span regulator [4,5]. These findings suggest that loss of H3K27me3, a repressive mark associated with regions of facultative heterochromatin, is not only associated with aging but may in fact be causally involved in the aging process. Recent genetic studies in �ies and worms have