Colorectal cancer (CRC) arise from multi-step carcinogenesis due to genetic mutations and epigenetic modifications of human genome. Genetic mutations and epigenetic modifications were originally established as 2 independent mechanisms contributing to colorectal carcinogenesis. However, recent evidences demonstrate that there are interactions between these 2 mechanisms. Genetic mutations enable disruption of epigenetic controls while epigenetic modifications can initiate genomic instability and carcinogenesis. This review summarized genetic mutations and epigenetic modifications in colorectal carcinogenesis and molecular classification of CRC subtype based on genetic or epigenetic biomarkers for treatment response and prognosis. Molecular subtypes of CRC will permit the implementation of precision medicine with better outcome of management for CRC.

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