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In this study, we performed whole-exome sequencing to identify somatic mutations in 24 patients with newly diagnosed chronic phase CML who were registered in the JALSG CML212 study. We identified 191 somatic mutations other than the <jats:italic>BCR-ABL1<\/jats:italic> fusion gene (median 8, range 1\u201317). Age, hemoglobin concentration and white blood cell counts were correlated with the number of mutations. Patients with mutations \u2a7e6 showed higher rate of achieving major molecular response than those&lt;6 (<jats:italic>P<\/jats:italic>=0.0381). Mutations in epigenetic regulator, <jats:italic>ASXL1<\/jats:italic>, <jats:italic>TET2<\/jats:italic>, <jats:italic>TET3<\/jats:italic>, <jats:italic>KDM1A<\/jats:italic> and <jats:italic>MSH6<\/jats:italic> were found in 25% of patients. <jats:italic>TET2<\/jats:italic> or <jats:italic>TET3<\/jats:italic>, <jats:italic>AKT1<\/jats:italic> and <jats:italic>RUNX1<\/jats:italic> were mutated in one patient each. <jats:italic>ASXL1<\/jats:italic> was mutated within exon 12 in three cases. Mutated genes were significantly enriched with cell signaling and cell division pathways. Furthermore, DNA copy number analysis showed that 2 of 24 patients had uniparental disomy of chromosome 1p or 3q, which disappeared major molecular response was achieved. 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