Consistent with their finding and ours, we posit that while CD133+ GBM cells may be molecularly quiescent or clinically indolent before they undergo proliferative cell division (PCD) to produce CD133- progeny, it is probable that DRD4 signaling induces the self-renewal of CD133+ GBM cells, enhances PCD which facilitates tumor cell regeneration and disease recurrence in patients with GBM. Here, DRD4 is linked to neoplasm.