To establish the requirement for mitochondrial Fh1 in AML development in vivo, we transplanted control (Fh1fl/fl), control;FHCyt, and Fh1fl/fl;FHCyt;Vav-iCre Meis1/Hoxa9-transduced preleukemic cells into sublethally irradiated recipient mice (Fig. 6 A). The gene discussed is FLNB; the disease is acute myeloid leukemia.