A previous study identified four molecular subtypes of gastric adenocarcinoma19: tumors that are EBV positive (EBV), tumors with high levels of microsatellite instability (MSI), tumors that exhibit copy number instability (CIN), and tumor that are genomically stable (GS). We investigated the correlations between somatic mutation rates of the four cancer subtypes and epigenetic profiles of gastric tissue obtained from the Roadmap Epigenomics project29. In general, somatic mutation rates were negatively correlated with regions of open chromatin (DNaseI hypersensitivity) and histone marks of active promoters (H3K4me3) and enhancers (H3K27ac) (Fig. 1b). The depletion of somatic mutations in regions of open chromatin is likely due to enhanced accessibility to the DNA repair machinery30–32. Notably, somatic mutations in the EBV subtype were less correlated with histone features and replication timing compared to the CIN and GS subtypes, suggesting that additional mutational biases may exist in EBV infected tumors.