Colorectal cancer (CRC) is the third most common malignancy diagnosed globally and the fourth leading cause of cancer-related death worldwide, with its burden predicted to increase by 60% by 2030.1 CRC progresses through a well-defined adenoma-carcinoma sequence,2 whereby the stepwise acquisition of well-characterised genetic mutations (e.g. APC, KRAS, TP53) drives intestinal crypt dysplasia, followed by the development of colorectal tumours. This evidence concerns the gene KRAS and colorectal carcinoma.