This targeting strategy typically involves genetic modification of HSV-1 OV, such as knocking out the viral TK and ICP34.5 genes to improve the tumor-killing ability or modifying the promoter of ICP0 into a tumor-specific promoter [e.g., human telomerase reverse transcriptase, hypoxia-responsive, carcinoembryonic antigen CEA, prostate-specific antigen, alpha-fetoprotein, alpha-lactalbumin, and mucin1 promoters (DF3/MUC1)], enabling their specific replication in tumor cells [137,138]. The gene discussed is KLK3; the disease is neoplasm.