This pharmacodynamic interaction has been characterized at a molecular level, and may be explained by the DUSP6 mechanism (DUSP6 suppression followed by increased p53 phosphorylation) in BRAFV600E and p53WT melanoma cells, which leads to synergistic induction of the expression of genes encoding PUMA and BIM that increase apoptosis ratio and growth inhibition of melanoma cells [3]. This evidence concerns the gene BCL2L11 and melanoma.