Approximately 10 to 20% of CRC cases exhibit mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) status,6 stemming from DNA MMR gene inactivation (MLH1, MSH2, MSH6, and PMS2).7 Numerous studies have reported diminished or absent responses to fluorouracil-based ACT in dMMR CRC patients versus CRC patients with mismatch repair-proficient/microsatellite-stable/(pMMR/MSS).8,9. This evidence concerns the gene PMS2 and colorectal carcinoma.