For example, Zuber et al., Fenouille et al. and Benajiba et al. were able to demonstrate, using large-scale shRNA functional screening approaches, that inhibition of the bromodomain protein Brd4 leads to AML cell growth impairment on one hand, and that inhibiting the mitochondrial creatine kinase (CKMT1) pathway on the other hand leads to proliferation arrest and apoptosis in the EVI1-driven AML subtype [148,149,150]. The gene discussed is RUNX1; the disease is acute myeloid leukemia.