ETS1 and melanoma: Considering that opposite functions of ETS-1 have been already described and linked to the different biological contexts (Sato et al., 2001), it is likely that in melanoma cells the net establishment of a more aggressive phenotype could derive from undermining the nuclear unphosphorylated and, even more, the serine-phosphorylated ETS-1 fractions characterized by a significantly lower DNA affinity (Pufall et al., 2005).