The somatic mutation rate is correlated with epigenetic features such as histone modification and chromatin accessibility30, especially those derived from the cell type of origin of the cancer32. We compiled 36 gastric specific and 24 general chromatin features that potentially affect mutation rate in GC. These 66 histone modification profiles and chromatin accessibility profiles were obtained from Roadmap Epigenomics29 and in-house data. We obtained P-value signal tracks of 853 DNaseI and histone modification profiles of 111 primary tissues and cell types from the Roadmap Epigenomics project. Among them, 27 epigenetic profiles were derived from gastric related tissues. For the 24 histone marks that were not assayed in gastric-related tissues, we created meta histone modifications profiles by taking the median profile of each mark across all tissues and cell-types assayed. In addition, we included histone modifications profiles of H3K4Me1, H3K4me3, and H3K27Ac of 19 GC tumor/normal samples and 13 GC cell lines (FU97, KATO3, MKN7, NCC24, NCC59, OCUM1, RERF-GC-1B, SNU16, SNU1750, YCC3, YCC7, YCC21, and YCC22)24,25. We used the median signal of each histone mark over all tumor samples, all normal samples, and all cell lines, respectively.