Figure 3 shows that ATM was not involved in the phosphorylation of 4E-BP1 during differentiation. Furthermore, as the PI3-K, Vps34, has been identified as a direct target of KU55933, our study also suggests that this PI3-K plays no role in controlling mTORC1 during myogenic differentiation34. The Pim family kinases have also been shown to function in a rapamycin-insensitive way to mediate the phosphorylation of 4E-BP1 in AML cells42. To investigate whether Pim kinases have a role in 4E-BP1 phosphorylation in C2C12 cells, we used the Pim kinase inhibitor, SGI-1776.42,43. The gene discussed is ATM; the disease is acute myeloid leukemia.