KRAS and neoplasm: For example, PE can accurately repair mutations in driver genes (e.g., TP53, KRAS, and EGFR) to restore their normal functions; restore the cancer-suppressive functions of tumor suppressor genes (e.g., PTEN or BRCA1) by inserting or repairing their mutated sites; edit immune checkpoint genes (e.g., PD-1 or CTLA-4) to enhance the tumor-killing ability of T cells; and introduce specific oncogenic mutations in cell or animal models to introduce specific oncogenic mutations for studying the mechanisms of carcinogenesis and drug screening.