However, the latest research has pointed out that, under the pressure of anti-EGFR drugs, human CRC cells with mismatch repair proficient/microsatellite stable (pMMR/MSS) can manifest dMMR phenotype in a variety of ways, including downregulating the expression of mismatch repair (MMR) genes (MLH1, MLH2, and MLH6), homologous recombination genes (BBRCA2 and RAD51), and double-strand break repair gene EXO1, and gradually replacing high-fidelity DNA polymerase by low-fidelity DNA polymerases to participate in the DNA-replication process. The gene discussed is EGFR; the disease is colorectal carcinoma.