Together these results indicate the prostate cancer-associated mutations in SPOP can be categorized into the three groups as follows: type I SPOP mutants retain partial ATF2 binding, ubiquitination and degradation capacity; type II SPOP mutants lose ATF2 binding, ubiquitination and degradation capacity; and type III SPOP mutants also lose ATF2 binding capacity and ATF2 ubiquitination, but stabilizes ectopically co-expressed ATF2, suggesting a possible “dominant-negative effect”. This evidence concerns the gene ATF2 and prostate carcinoma.