Recurrent CDK12 mutations in breast and ovarian cancers are associated with defects in DNA repair.17 Silencing of CDK12 has been shown to activate the mitogen-activated protein kinase signaling pathway, leading to endocrine therapy resistance through loss of ER dependence.18 TET2 (tet-eleven translocation 2) from the TET family of DNA dioxygenases functions as DNA demethylases, antagonizing DNA methyltransferases-mediated DNA methylation and gene repression. Here, CDK12 is linked to ovarian cancer.