Although a great amount of research has been devoted to the genetic factors that directly affect aging, nongenetic control of aging has gained considerable interest lately as an important aspect in getting awareness of the process of aging. Nongenomic modifications that affect gene expression and modify the chromatin structure are referred to as epigenetic alterations, and are generally defined as alterations in genomic regulation not directly encoded by DNA, i.e., alterations that do not change the DNA sequence, but instead control gene operations. Such changes take place when methyl groups are added to or removed from DNA (DNA methylation/demethylation), when post-translational modifications are made to the histones, and upon chromatin remodeling (Figure ). These changes may occur upon aging and/or exposure to environmental factors, they can be also inherited. They can also be called epimutations. The enzymatic systems ensuring the generation and maintenance of epigenetic alterations include the enzymes DNA methyltransferases, histone acetylases, deacetylases, methylases and demethylases. They also include proteins involved in chromatin remodeling. Epigenetic alterations are profoundly involved in the process of aging, resulting in disturbances in the wide-ranging genome architecture, thus understanding the epigenome holds promise for amending agerelated pathologies and prolonging healthy lifespan. In addition to age-related epigenomic changes, many other systems become dysfunctional with age. Noteworthy, chromatin and transcription regulation have been identified to play major roles in the age-associated symptoms of these aging hallmarks. Given the reversible nature of epigenetic pathways, their understanding provides a promising approach for therapeutics against age-related decline and disease. As mentioned above, epigenetic alterations take place when methyl groups are added to or removed to a cytosine base (C) of DNA or when modifications are made to proteins called histones that bind to the DNA in chromosomes. DNA methylation produces DNA condensation, the form in which genes are not being transcribed. DNA methylation in mammals primarily occurs on the C5 of the cytosine base (5 methylcytosine, 5-mC) of CpG dinucleotides. Nearly 70-80% of CpG dinucleotides are methylated in somatic cells. Methylation levels change throughout life, but generally tend to decrease upon aging. Global 5-methylcytosine (5mC) variations have been first described during aging in rats. DNA methylation affects a wide range of developmental and pathological processes. Further on, vast literature has documented genome-wide DNA methylation changes that occur in response to aging across multiple species. Although aging is largely correlated with changes in DNA methylation, the relationship between DNA methylation and aging is complicated. The general trends involve largescale hypomethylation (non-CpG islands) and regions of hypermethylation (primarily CpG islands) upon aging. It is currently believed that DNA methylation biomarkers can verify biological age throughout the entire human lifespan. This phenomenon, known as epigenetic clock, is based on CpG sites (cytosine and guanine bases separated by only one phosphate group in the DNA sequence) associated with age and the methylation profile of which can be used as an accurate indicator of biological age. Moreover, DNA methylation-based clocks are suggested as biomarkers of early disease risk and as forecasters of life expectancy and mortality. Thus, the Horvath Clock defines a pattern of DNA methylation changes and considers the global decline in genomic CpG methylation as a well-documented predominant event in aging. A strong causative link between DNA and H3K9 methylation and aging is considered likely , however, the mechanisms underlying age-related DNA methylation alterations and aging mechanism are yet to be fully understood.