The most common abnormality found in colorectal cancer is mutation in the Wnt signaling pathway, which increases cell signalling activity. The mutations can be inherited or acquired. The most commonly mutated gene is the APC gene, which results in accumulation of the β-catenin protein. β-catenin activates the transcription of various proto-oncogenes that are responsible for normal cell renewal and differentiation, but when overexpressed can cause cancer. Many other muta- tions, other than in the Wnt signaling pathway, are found in colorectal cancer, and include mutations in the TP53 gene that controls normal cell division and death, and mutations in genes responsible for programmed cell death, such as the gene encoding transforming growth factor (TGF)-β and DCC (deleted in colorectal cancer). Other genetic abnormalities include overexpression of oncogenes, including genes encod- ing the proteins KRAS (Kirsten rat sarcoma homologue), RAF (rapidly accelerated fibrosarcoma) and PI3K (phospho- inositide 3-kinase), which lead to increased cell proliferation, and inactivation of tumour suppressor genes, such as PTEN (phosphatase and tensin homologue), which normally inacti- vates the PI3K signalling pathway. In addition to gene mutations, colorectal cancers fre- quently exhibit epigenetic alterations – cellular or physiolog- ical effects resulting from external or environmental factors that switch genes on or off. Epigenetic alterations can affect hundreds of genes and include changes in the expression of microRNAs (miRNA), hypermethylation or hypomethyl- ation of CpG islands of protein-encoding genes, and alter- ations in histones and chromosomal architecture, all of which can influence gene expression.