In the later stages of SVA infection, the viral 3Cpro activates caspase to cleave p65, resulting in a significant decrease in the transcriptional activity of NF-κB (44).Moreover, apoptotic cells can promote the release and spread of SVA from infected cells, thereby facilitating a broader “tumor-killing” effect within the tumor (44). The gene discussed is NFKB1; the disease is neoplasm.