Epigenomic changes have been considered a potential missing link underlying phenotypic variation in quantitative traits but is potentially confounded with the underlying DNA sequence variation. Although the concept of epigenetic inheritance has been discussed in depth, there have been few studies attempting to directly dissect the amount of epigenomic variation within inbred natural populations while also accounting for genetic diversity. By using known genetic relationships between Brachypodium lines, multiple sets of nearly identical accession families were selected for phenotypic studies and DNA methylome profiling to investigate the dual role of (epi)genetics under simulated natural seasonal climate conditions. Despite reduced genetic diversity, appreciable phenotypic variation was still observable in the measured traits (height, leaf width and length, tiller count, flowering time, ear count) between as well as within the inbred accessions. However, with reduced genetic diversity there was diminished variation in DNA methylation within families. Mixed-effects linear modelling revealed large genetic differences between families and a minor contribution of epigenomic variation on phenotypic variation in select traits. Taken together, this analysis suggests a limited but significant contribution of DNA methylation towards heritable phenotypic variation relative to genetic differences.Recently, there has been great excitement investigating the role of possible epigenomic sources of variation, in the form of stable DNA or histone modifications, which may act alongside, or independently, of traditional genetic variation. A range of population-level studies have reported substantial diversity between different genetic backgrounds [4][5][6][7][8][9]. In certain cases, measures of DNA methylation were combined with genetic variation identifying genetic factors that can influence chromatin between populations and geographical locations [6,[10][11][12]. Results often highlight the covariation of genetic variation with chromatin state, transposable element (TE) methylation, and differential cytosine methylation among accessions. Nonetheless, a small portion of geneticallyindependent methylation variation, often in the CG context and in promoter regions, may contribute to phenotypic variance [6,[13][14][15].