Phosphorylation of TBK1, a key target of RALB signaling, was decreased after Dox-mediated NRAS(V12) suppression in de novo NRD AML, but was maintained at higher levels in relapsed NRI AMLs, even in the absence of NRAS(V12) expression (Figure 3a). This evidence concerns the gene RALB and acute myeloid leukemia.