Non-canonical upstream activation of AR in melanoma is an important consideration for future studies of androgen- and AR-regulated melanomagenesis, as independent of its canonical ligand DHT, AR is known to be phosphorylated and activated by other factors (e.g., AKT, HER2, and ACK1 kinases) in prostate cancers77–80. This evidence concerns the gene AKT1 and melanoma.