Thus, the tumor-suppressive activities (e.g., immune surveillance, anti-tumorous biology) of both Maspin and p53 were integrated by an HDAC1-mediated interaction and formed a “self-propelling” antitumor mechanism to prevent the digressional process until discharging the cellular stress and consequentially fine-tuning the epithelial homeostasis (Figure 3). The gene discussed is SERPINB5; the disease is neoplasm.