JUN and neoplasm: For example, CDK8 inhibitors enhance IL-10 production during innate immune activation in human and mouse primary macrophages and dendritic cells (DCs) via diminished phosphorylation of the c-Jun subunit of the AP-1 transcription complex.21 CDK8/19 can also inhibit gene expression of SE-associated lineage-controlling TFs identified in related CD14+ monocytes, including the tumor suppressors IRF1, IRF8, CEBPA, and ETV6, and the kinase activity of CDK8/19 can be pharmacologically targeted as a therapeutic approach to AML.26