Nuclear export and phosphorylation are two major approaches causing the loss of RB1's tumor suppressor function.[25, 32] XPO1 was reported to promote the proliferation of glioma cells by increasing the nuclear export of RB1.[25] To validated whether XPO1 functions through RB1 nuclear export in BLBC cells, we knocked down wild‐type RB1[33] in HCC1806 and SUM149PT cells and found that cell proliferation was significantly increased (Figure3A,B). The gene discussed is RB1; the disease is central nervous system cancer.