Large genomic datasets have provided some insights as to the relative frequency of AKT-isoform-specific alterations; the activation of mutations or gene amplification of AKT1 and AKT2 are more common in BRAFV600E mutant and PTEN-null melanomas [28,29], whereas AKT3 amplification is more common in BRAFWTPTENWT tumors [26], although AKT3 has also demonstrated co-operativity with BRAFV600E to induce murine melanoma development [30]. This evidence concerns the gene PTEN and melanoma.