AKT1 and melanoma: Alternatively, these pathways can be constitutively activated in melanoma cells due to somatic mutations of their components [e.g., BRAFV600E, NRASQ61R, Akt1/3E17K, Akt1Q79K, or point missense mutations, insertions and deletions in the coding region of the tumor suppressor gene phosphatase and tensin homolog (PTEN)] (3,23–26), or by epigenetic modifications of their downstream effectors, like PTEN methylation (26).