Without a doubt, PTEN status is critical in determining the functional outcome of pharmacologic MEK inhibition in melanoma and in cellular contexts in which PTEN is genetically unaltered, MEK blockade induces a cross-talk mechanism that leads to PTEN protein induction, playing an important, albeit not exclusive, role in the anti-tumor and anti-angiogenic activities of MEK inhibitors (106). This evidence concerns the gene PTEN and neoplasm.