Forced expression of miR-22 remarkably inhibited progression of MLL-AF9-, AE9a- or FLT3-ITD/NPM1c+-induced AML in secondary recipient mice (Fig. 2a–d), resulting in largely normal morphologies in PB, BM, spleen and liver tissues (Fig. 2b; Supplementary Fig. 2c). The gene discussed is FLT3; the disease is acute myeloid leukemia.