Upon infection, viruses can also inhibit apoptosis of host cells and dysregulate caspases by encoding homologs of the anti-apoptotic proteins, such as Bcl-2, blocking apoptosis signals by triggering expression of the tumor necrosis factor (TNF) family members, or by inactivating IFN-induced protein kinase R (PKR) or p53 pathways that result in tumor formation [29,30,31]. Here, TNF is linked to neoplasm.