Specifically, in Lck-MyrAkt2 mice, constitutively active Akt2 alone may serve as such a potent oncogenic factor that Myc activation, either directly via a Myc translocation or indirectly through its transcriptional activation by Dlx5, is sufficient as a “second hit.” In contrast, in Lck-Dlx5 mice, which have a longer tumor latency than Lck-MyrAkt2 mice, multiple oncogenic factors, including Notch1/3, Irs2, Cyclin D, and Myc, appear to be required to initiate tumor formation. The gene discussed is LCK; the disease is neoplasm.