To place the four-fold increase into perspective in PCa disease progression, Barbieri and co-workers identified a plausible PCa subtype consisting of mutant SPOP in combination with a lack of ETS family gene rearrangements.48 In the Barbieri datasets, the increase of mutant SPOP from early to metastatic CRPCa is two-fold (6–15%). The gene discussed is SPOP; the disease is posterior cortical atrophy.