IDH1 and acute myeloid leukemia: 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.