A major breakthrough in medical oncology was the discovery of immune checkpoints and the development of immune checkpoint inhibitors. Neoadjuvant checkpoint inhibition is a promising new approach to manage some melanomas and lung cancers, and is also being explored in other cancers. 1 This approach relies on the ability of neoadjuvant immune checkpoint inhibitors to induce T-cell expansion at early stages of cancer when T-cell function is less impaired, and it has the potential to reduce tumour size before surgery. The efficacy of immune checkpoint inhibitors is now clear for patients with advanced microsatellite instability-high or DNA mismatch repair-deficient colorectal cancer. 2, 3 This phenotype is observed in approximately 15–18% of stage II, 9–10% of stage III, and 4–5% of stage IV colorectal cancers. 3, 4 In these patients, mismatch repair-deficient or microsatellite instability-high disease has been shown to be a favourable prognostic marker in stage II disease but its prognostic value is more controversial among stage III and stage IV colorectal cancers. The standard treatment of stage II and III mismatch repair deficiency or microsatellite instability-high colon cancers is surgical resection of the primary tumour, followed by adjuvant chemotherapy combining fluoropyrimidine and oxaliplatin for stage III cancers. 4, 5