We implicated the oncogenic potential of these fusion genes because our SNV profiling determined that the presence of fusion genes was mutually exclusive with the presence of oncogenes in CRC patients, exception of one patient expressing TMOD3-MAPK6 (P = 0.029), concurrent with previous reports wherein tumour samples harbouring fusion genes tended to have significantly fewer oncogene mutations.27, 28 However, cancer progression of the patient with TMOD3-MAPK6 may be affected by oncogene and tumour suppressor gene mutations involving POLE, in addition to the fusion gene.4 This evidence concerns the gene POLE and neoplasm.