A similar scenario may be also at play in neuronal progenitors, resulting in the formation of medulloblastomas, and in epithelial cells of the gastrointestinal tract, where productive infection does not occur; the prevention of apoptosis may result in time for T-Antigen to dysregulate the Wnt signaling pathway, by binding and translocation β-catenin to the nucleus, where it activates c-Myc and Cyclin D. Figure 6 depicts a diagram of this hypothetical model of mechanisms utilized by JCPyV in both, PML and brain tumorigenesis. The gene discussed is PML; the disease is infection.