Two independent studies have demonstrated a therapeutic vulnerability of EVI1high AMLs towards the inhibition of ERG signaling.50,51 In the EVI1high leukemic cells, knockdown of ERG led to a decrease in proliferation and an increase in apoptosis, and also induced differentiation.50 However, achieving a pharmacological inhibition of ERG in AML patients, as is the case for many transcription factors, remains a challenge and is currently still a subject of research and development.117. The gene discussed is ERG; the disease is acute myeloid leukemia.