Based on the VP-MCC-like tumor tumorigenic pathway supported by the obligatory extremely low global DNA methylation unique for “late-hPGC” state and the known intrinsic pluripotency-teratoma coupling with teratoma components exhibiting much higher global DNA methylation in VP-MCC-like tumor (+) tumors (Figure 4B), an independent tumorigenic pathway is favored for the teratoma components of VP-MCC-like tumor (+) tumors, involving multi-lineage somatic differentiation from a pluripotent precursor [20]. The gene discussed is MCC; the disease is teratoma.