Two studies uncovered distinct molecular mechanisms that sustain acute myeloid leukemia (AML) survival and progression. One report identified THRAP3 as a promoter of ferroptosis resistance through SLU7‑dependent splicing, providing a potential vulnerability to ferroptosis‑inducing therapies. The mechanism highlights splicing regulation as a targetable axis in AML. Separately, researchers found that the noncoding RNA RPPH1 drives high‑risk AML by activating NF‑κB signaling and skewing immune responses toward Th17‑mediated inflammation. Both studies provide candidate biomarkers and therapeutic strategies—splicing modulators, ferroptosis agonists, and NF‑κB pathway inhibitors—that could feed combination regimens in next‑generation AML trials.