Suicidal behaviors (SB) can be seen as a complex interaction between genetic and environment all along life (e.g., childhood trauma, lifestyle) and epigenetics could be the key for a better understanding of this complex pathophysiology. Three main epigenetics changes are currently identified: DNA methylation, non-coding RNA (e.g., microRNA) and histone modifications (e.g., acetylation). Studies on epigenetic in SB are mainly focused on hypothalamic–pituitary–adrenal axis (HPA axis), neurotrophic system and polyamines system. In this chapter we reviewed some studies on epigenetics changes of the HPA axis, of the neurotrophic system and of the polyamines system in SB. We also succinctly reviewed some studies on epigenetics of other systems involved in SB and results from genome-wide DNA methylation studies. According to post-mortem studies and studies in living subjects, numerous epigenetics changes from different systems seem to be involved in pathophysiology of SB (e.g., hypermethylation of SKA2, NR3C1, TRKB). In addition, these epigenetics changes are associated with difference in genes expression in suicidal subjects contributing to deregulation of systems involved in SB. Thanks to genome-wide DNA methylation news genes of interests are emerging to study in SB (e.g., RARRES3, PUS3, CXCL8). Yet, epigenetics studies in SB are needed to replicate previous results, to study deeper new genes of interests, to better understand pathophysiology of SB and to find news therapeutics targets. However, waiting, some epigenetics modifications could be promising biomarkers helping clinicians to identify patients at suicidal risk (e.g., SKA2 and BDNF methylation in the whole blood seem to be associated with suicidal ideation and suicide attempt). It is primordial to continue to study epigenetics of SB, a very promising key of the understanding of these disorders.