Often considered one disease, sporadic colorectal cancer (CRC), accounting for 95% of CRC cases, is a heterogeneous disease arising from different sets of genetic and epigenetic alterations.1 The most established underlying molecular pathological subtypes of CRC are characterised by microsatellite instability (MSI) (prevalence 15% in sporadic CRC), CpG island methylator phenotype (CIMP-high, 20%),2 B-Raf proto-oncogene serine/threonine kinase gene mutations (BRAF mutations, 10%) and Kirsten rat sarcoma viral oncogene homologue gene mutations (KRAS mutations, 30–50% of sporadic CRC cases). The gene discussed is BRAF; the disease is colorectal carcinoma.