Lastly, OVs that are engineered to exploit specific gene mutations like mutated P53, Ras, and Rb genes in tumors [165] or that use tumor-specific promoters to enhance their tumor-selectivity may result in a sub-optimal therapeutic efficacy because of the diversity in the level of expression of these specific mutated genes in tumor cells [167,168,169]. The gene discussed is TP53; the disease is neoplasm.