Epigenetic states are initiated by environmental cues, developmental stimuli, cellular events and their sequelae and mediated by various cellular mechanisms including histone modifications, DNA methylation signals, non-coding RNAs and transcription factor networks (Bonasio and Reinberg, 2010). These mechanisms ultimately shape the chromatin architecture and fine-tune the transcriptome so that it can respond even in the absence of the initiating cue. This results in an “epigenome” that co-exists with the genome and is stably maintained in mitotic and post-mitotic cells, such as neurons, in a self-sustaining fashion (Dulac, 2010). A process that is critical for normal cellular physiology and function. Environmental factors, such as ethanol, usually dysregulate neuronal functions via epigenetic modifiers (Moonat et al., 2013) and lead to positive and negative affective states of addiction (Pandey 2004; Koob & Volkow, 2010; Arora et al., 2013). Epigenetic targets therefore hold the promise for improved disease management, especially for a disease such as alcoholism whose endophenotypes are under complex epigenetic regulation. A deeper knowledge of the epigenomics of alcoholism will enable us to identify the checkpoints and the processes that take us down the vicious path of addiction and the interventions necessary to reverse that trajectory (Figure 3).
