MTOR and acute lymphoblastic leukemia: Thus—and recalling our much earlier xenograft experimental finding that RASmt Reh cells grew much more slowly than control Reh cells—our metabolism-based investigation led us from the observation of differential Met levels, to validation of increased polyamine biosynthesis, and ultimately to confirmatory evidence about growth-related impacts of differentially activated mTOR signaling in KRAS-G12D mutation-bearing B-ALL cells.