TP53 and neoplasm: In addition, for the E1B55K-deficient shDaxx downregulation experiments, p53 functionality (A549 cells with wild-type p53) was necessary for efficient tumor regression, supporting the view that shDaxx downregulation with functional p53 enhances apoptosis, promotes adenoviral replication, and increases late viral gene expression5 rather than the competing view that successful adenovirus replication requires inactivation of p53.