Promising results have also been achieved using an oncolytic HSV-2 with a deletion in the protein kinase domain of the viral ICP10 gene, which specifically targets the activated Ras signaling pathway in tumor cells [131] or using HSV-1 mutants lacking ICP34.5, capable of killing OC cells that lack p53 function, resist apoptosis, and/or are chemotherapy-resistant [132]. The gene discussed is TP53; the disease is neoplasm.