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. The gene discussed is POU3F2; the disease is neoplasm.