Colorectal cancer (CRC) is one of New Zealand’s most common cancers and the second highest cause of cancer mortality. While the development of CRC can stem from the accumulation of genetic mutations over time, emerging research has demonstrated that epigenetic alterations such as aberrant DNA methylation is strongly associated with the initiation and progression of CRC. Individuals with chronic inflammatory conditions of the bowel, such as inflammatory bowel disease (IBD) and serrated polyposis syndrome (SPS), are at a significantly increased risk of developing CRC. While the functional relationship between chronic inflammation and cancer development is now widely accepted, the precise molecular mechanisms involved remain unclear. Immune cells release oxidants in response to infectious agents or irritants into the extracellular environment, which can have cytotoxic effects when present in high and sustained quantities, such as in a state of chronic inflammation. We have shown that the neutrophil oxidants, hydrogen peroxide and glycine chloramine, can interfere with the maintenance of DNA methylation patterns during cellular replication. DNA methylation is imperative in the regulation of gene expression, including cancer-mediating tumour suppressor genes and oncogenes. Profiling DNA methylation patterns in CRC is a useful tool for understanding the heterogeneity of malignant phenotypes. Furthermore, a better understanding of the mechanisms that cause DNA methylation change may facilitate the development of targeted therapies and precision medicines, leading to improved clinical outcomes.