This dependency was mirrored in vivo, where residualSTAT1SER727 phosphorylation remained sensitive to inhibition,implicating CDK19 in contributing the remaining ∼25% of activity.Interestingly, a discrepancy emerged between in vitro and in vivodata: although CDK8-knockout clones were resistant to growth suppressionin vitro, tumor xenografts derived from the same clones remained responsiveto inhibitor treatment in vivo. This evidence concerns the gene CDK19 and neoplasm.