However, as we did not assess their expressionin the in vivo tumor xenografts, we cannot exclude the possibilityof compensatory upregulation of CDK19 in the CDK8-knockout tumors.Nonetheless, our findings support the hypothesis that functional redundancybetween CDK8 and CDK19 may be enhanced under tumor growth conditions,enabling CDK19 to partially compensate for the absence of CDK8 inthe in vivo context (summarized in Table ). The gene discussed is CDK8; the disease is neoplasm.