Given that in PCa the SPOP mutations are hemizygous in nature and G3BP1 binds to wild-type SPOP but not SPOPF133V mutant, our results suggest that G3BP1 adds another layer of negative regulation of remaining SPOPWT allele on top of the existing tumor-promoting effect of SPOPF133V. The gene discussed is SPOP; the disease is posterior cortical atrophy.