Chemical inhibition of CDK12 with THZ531 leads to decreased cancer progression by downregulating AR signaling and suppressing super-enhancer-associated oncogene expression.413 Moreover, CDK12 loss mediates genome instability in prostate cancer and may lead to higher neoantigen levels and T-cell infiltration, suggesting it potential suitability as biomarker for immunotherapy.409. The gene discussed is AR; the disease is prostate carcinoma.