With both approved and investigational therapies available to target oncogenes (e.g., FLT3, IDH1/2, NPM1c/Menin inhibitors) responsible for regulating the expression and/or post-translational modifications (e.g., methylation, acetylation, glycosylation, ubiquitination) of proteins in AML cells, it is critical to determine if targetable driver mutations are important for the increased expression of immune checkpoints in AML cells. The gene discussed is FLT3; the disease is acute myeloid leukemia.