The field of epigenetics provides neurobiologists with candidate mechanisms for experience-dependent changes in gene transcription. The ability to realize the potential of epigenetics in defining the causal pathways lying between environmental signals, transcriptional regulation and neural function will depend on moving beyond correlational studies focusing on individual epigenetic marks. Here we attempt to provide a conceptual framework for integrative research on nucleotide sequence, chromatin modifications, RNA signaling and their interactions in understanding experience-dependent phenotypic plasticity. Studies in genomic imprinting may serve as an existing model for such approaches.