CDK8 may control the cell cycle inhibitor p27 by driving its phosphorylation at the T187 residue, creating a priming site for Skp2-mediated p27 ubiquitination and degradation, thereby promoting cell cycle progression and tumorigenesis.369 Pharmacological (Senexin A and B) or genetic inhibition of CDK8 suppresses both the transcriptional (e.g., GREB1 and EGR3 genes) and mitogenic effects of estrogen in ER-positive breast cancer cells, partially suppresses HER2+ breast cancer tumor growth and potentiates the effects of HER2-targeting drugs, overcoming lapatinib resistance.370. This evidence concerns the gene ERBB2 and neoplasm.