Importantly, several lines of evidence indicate that the ERK pathway, which is commonly deregulated in melanomas due BRAF or NRAS mutations, can contribute to silencing the MST2 pathway proapoptotic signal through different mechanisms: (i) RAF1 and mutant BRAFV600E can block LATS1 activity by direct binding and inhibition of MST kinases [18, 19]; (ii) activated AKT inhibits MST2 by direct phosphorylation [20]; (iii) mutant NRAS can inhibit MST2 activation, potentially through AKT activation [21]. Here, BRAF is linked to melanoma.