As such, we believe that the increased proliferation and tumor-initiation frequency observed in our BrafV600E/PtenF/+ model arising as a consequence of the reduction of Brn2, is likely to occur as a consequence of the ability of Brn2 to activate Pten expression and suppress PI3K signaling either directly or potentially indirectly via Mitf repression during early melanomagenesis. Here, PTEN is linked to neoplasm.