In line with these results, MLL-AF9 strongly stimulated the development of AML progenitors, with similar efficiency both in Yapflox/flox/Tazflox/flox and in YapΔ/Δ/TazΔ/Δ cells, while no CFU-stimulating activity was detected by N-RASG12D transduction in either control or Yap/Taz-deleted HPCs (Fig. 2a). This evidence concerns the gene MLLT3 and acute myeloid leukemia.