ERK-mediated phosphorylation enhances the stability of MCL-1 and appears to confer chemo-resistance in breast cancer cell lines, whereas CDK1-mediated phosphorylation targets MCL-1 for degradation during mitotic arrest, and GSK-3-mediated phosphorylation targets MCL-1 for proteosome-mediated degradation [75–78]. This evidence concerns the gene MCL1 and breast carcinoma.