Consistent with these studies, the present study has clearly demonstrated that RSK1 activated by FLT3-ITD plays a critical role in phosphorylation of Bad on S75 corresponding to S112 in mice, because it was rapidly abrogated by LJH685 in parallel with inhibition of RSK NTKD in MV4-11 cells, was inhibited by LJH685 also in primary FLT3-ITD-positive AML cells from one patient we could examine, and was remarkably reduced or enhanced by RSK1 deletion or overexpression, respectively, in MV4-11 cells (Figure 5A,B,E–G). The gene discussed is FLT3; the disease is acute myeloid leukemia.