Although this was not the top upregulated gene, given the specificity of PLK1 overexpression to clonal RAS mutant pCMML, along with prior work using a genome-wide RNAi screen that had shown sensitivity of RAS mutant cells to PLK1 inhibition and that RAF1/CRAF has shown to have direct interactions (MEK independent) with PLK1 at centrosomes and spindle poles during G2/mitosis, and the fact that phase III trials with PLK1 inhibitors (volasertib) had already been completed in AML, we chose to further assess the functional and therapeutic relevancy of this mitotic checkpoint kinase18,19. The gene discussed is RAF1; the disease is acute myeloid leukemia.