For example, the pan CDK inhibitor dinaciclib restored sensitivity to navitoclax- and venetoclax-mediated apoptosis in resistant lymphoma cells via inhibition of MCL-1 phosphorylation by CDK2/Cyclin E, which in turn led to the destabilization of MCL-1 protein and release of BIM from MCL-1 (228). Here, MCL1 is linked to lymphoma.