We previously found that primary AML samples have increased levels of RALB-TBK1 signaling compared with normal blood mononuclear cells from healthy mobilized peripheral blood donors.37In vitro treatment of a panel of AML samples with dinaciclib uniformly resulted in decreased phosphorylation of TBK1 and increased cleavage of CASP3, while normal mononuclear cells from healthy donors were relatively insensitive to dinaciclib treatment (Figure 6). This evidence concerns the gene TBK1 and acute myeloid leukemia.