Anorexia Nervosa (AN) is a young-onset psychiatric illness, for which the etiology remains unknown and presents a high heritability. Thus, the genetic component is estimated to be 70%. To identify the vulnerability genes to AN, different approaches of molecular genetic are performed, including linkage analysis, the candidate gene association study and, the Genome-Wide Association Study (GWAS). Some polymorphisms of candidate genes, such as the BDNF gene that encodes for the brain-derived neurotrophic factor, were found associated with AN in several studies. In addition to the DNA polymorphisms, there are several other changes around the DNA information, like methylation or the histone modifications, named epigenetic, that modulate the transcription of genes. Thus, first descendents after the Dutch famine in the Second World War have showed a higher risk of impaired glucose tolerance in adulthood. And women exposed to famine in utero presented DNA methylation differences but without link of cause or consequence between famine event and epigenetic changes. To date, only few events of methylation in specific candidate genes have been investigated in AN. Thus, an hypermethylation of the DRD2 gene's promoter was found associated with a downregulation of this gene expression in AN compared to healthy control women (HCW), using leucocytes. While a hypermethylation of the DAT1 promoter was observed correlated with an upregulation of this gene expression. Another study has showed no difference of the methylation level of the Proopiomelanocortin (POMC) promoter between the goups of HCW, underweight AN (acAN) and weight-recovered AN (recAN). But, the expression of POMC was significantly higher in acAN compared to recAN and HCW, and correlated with the leptin levels. These studies suggest that both the etiology and the pathologic consequences of AN could be derived by epigenetic factors, such as the methylation.