Niche theory is one of the central organizing concepts in ecology. Generally, this theory defines a given species niche as all of the factors that effect the persistence of the species as well as the impact of the species in a given location (Hutchinson 1957; Chase 2011). Many studies have argued that phenotypic plasticity enhances niche width because plastic responses allow organisms to express advantageous phenotypes in a broader range of environments (Bradshaw 1965; Van Valen 1965; Sultan 2001). Further, species that exploit habitats with fine-grained variation, or that form metapopulations, are expected to develop broad niche widths through phenotypic plasticity (Sultan & Spencer 2002; Baythavong 2011). Although a long history of laboratory, greenhouse and reciprocal transplant experiments have provided insight into how plasticity contributes to niche width (Pigliucci 2001), recent advances in molecular approaches allow for a mechanistic understanding of plasticity at the molecular level (Nicotra et al. 2010). In particular, variation in epigenetic effects is a potential source of the within-genotype variation that underlies the phenotypic plasticity associated with broad niche widths. Epigenetic mechanisms can alter gene expression and function without altering DNA sequence (Richards 2006) and may be stably transmitted across generations (Jablonka & Raz 2009; Verhoeven et al. 2010). Also, epigenetic mechanisms may be an important component of an individual’s response to the environment (Verhoeven et al. 2010). While these ideas are intriguing, few studies have made a clear connection between genome-wide DNA methylation patterns and phenotypic plasticity (e.g. Bossdorf et al. 2010). In this issue of Molecular Ecology, Herrera et al. (2012) present a study that demonstrates epigenetic changes in genome-wide DNA methylation are causally active in a species’ ability to exploit resources from a broad range of environments and are particularly important in harsh environments.