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Mutant NRAS^G12V drives acute myeloid leukemia (AML) cell proliferation and self-renewal in a mutually exclusive manner. Previous studies demonstrated that AML cell proliferation and self-renewal are associated with differential NRAS^G12V transcript levels, but whether different NRAS^G12V protein levels dictate proliferative versus self-renewal phenotypes is not known. To address that knowledge gap, Kurata and colleagues engineered AML cell lines in which tetracycline-inducible NRAS^G12V expression levels are tunable using various doxycycline doses. The authors found that moderate NRAS^G12V protein expression promotes AML cell proliferation, whereas higher NRAS^G12V protein expression facilitates AML cell senescence and self-renewal. Using mass cytometry, the authors showed that abundances of several downstream NRAS^G12V effectors, including known stemness mediators such as β-catenin, increase in a dose-dependent fashion, whereas others, such as phosphorylated STAT1, are not dose-dependent. Overall, this study demonstrates that differential NRAS^G12V protein levels disparately drive AML cell proliferation and...