Conversely, in the setting of phosphatase and tensin homolog (PTEN) loss, conditional expression of mutant SPOP in the prostate induced the appearance of high-grade prostatic intraepithelial neoplasia (PTEN heterozygous background) and invasive poorly differentiated carcinoma (PTEN homozygous background), suggesting that mutant SPOP is able to cooperate with PTEN to drive carcinogenesis [13]. This evidence concerns the gene PTEN and prostate intraepithelial neoplasia.