PTP4A3 and neoplasm: Importantly, since mitosis-independent PGCCs possess the ability to exit TIS via de-polyploidization to generate the seed population for tumor repopulation and disease recurrence2,9, our finding that PRL3-zumab can inhibit the recurrence of PRL3+ tumor which is possibly hyperploid in nature and potentially represent a step forward in targeting tumor ‘dormancy’ by abolishing this classically chemoresistant, residual self-renewing PGCC population.