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. This evidence concerns the gene BRCA1 and neoplasm.