We observed that full length HA-SIX1 and SD were able to interact with SENP3, indicating that the N-terminal (1–128) of SIX1 is required for the binding of SENP3.Taken together, these results suggest that SENP3 can interact with the SD domain of SIX1 in the nucleus of PCa cells. The gene discussed is SENP3; the disease is posterior cortical atrophy.