Furthermore, MCPyV’s inability to induce non-seminomatous germ cell cancer-like transformation also suggests that the teratoma components observed in hPGCLC_A4_L82-derived VP-MCC-like tumor (+) tumors have arisen directly from an in vivo parthenogenic derivative competent for teratoma formation, from hPGCLC_A4_L82 modeling early-hPGCs [35] as spontaneous germline developmental progression in vivo to a “late-hPGC” state would have resulted in a parthenogenic derivative incapable of teratoma formation [20]. The gene discussed is MCC; the disease is neoplasm.