Consistent with this, ablation of <i>Cdk12</i> in prostate organoids with concurrent <i>Trp53</i> loss promotes their proliferation and ability to form tumors in mice, while <i>Cdk12</i> knockout in the <i>Pten</i>-null prostate cancer mouse model abrogates tumor growth. This evidence concerns the gene PTEN and prostate carcinoma.