Through this approach, 20% of prostate cancers were found to display mutations in genes that encode epigenetic modifiers or chromatin remodeling genes, more frequently observed in tumors that lack an ETS fusion; recurrently mutated genes were observed in the ubiquitin protease and ligase gene family, of which SPOP is a member, with mutations found in USP28 (1.4%), UPS7 (1.2%), and CUL3 (1.3%) genes; AR-genes are mutated in ~12% of these tumors (AR, 5%; SPEN, 2.4%; NCOR1, 2.5%; and NOCR2, 1.9%); WNT pathway was altered in 25% of samples, with predominant alterations of PTEN (16%) [61]. This evidence concerns the gene SPOP and prostate cancer.