Kampo et al. (2019) demonstrated that Nav 1.5 functional activities may play a role in BmK AGAP-mediated inactivation of the NF-κB/Wnt/β-catenin signaling pathway to inhibit stemness and epithelial–mesenchymal transition of breast cancer cells in vitro and in vivo by downregulating PTX3. In this study, decreased expression of VEGF post rBmK AGAP treatment correlated with decreased Ki-67, p65/NF-κB, and NF-κB DNA binding and transcription activity inhibiting breast tumor growth (Figure 7). The gene discussed is MKI67; the disease is breast cancer.