With our focus being the development of therapeutic approaches to avert AML development, we used extant therapeutics to target selected vulnerabilities—namely, the citrate transporter SLC25A1 (with CTPI2) and ETC complex I component NDUFB11 (with metformin or IACS-010759)—and found that these treatments reversed the selective growth advantage of Dnmt3aR882H over WT LT-HSC in transplanted recipients. The gene discussed is NDUFB11; the disease is acute myeloid leukemia.