Since our data strongly support that BMI1 regulates AR signaling in CRPC cells, and treatment of CRPC is still limited, we first used a castration-resistant VCaP xenograft mouse model32 to evaluate the therapeutic potential of BMI1 inhibition in CRPC, and PTC209 treatment significantly reduced tumor growth compared to vehicle control treatment (Fig. 6c). The gene discussed is BMI1; the disease is neoplasm.