Mutations in RUNX1 and G-CSF receptor (CSF3R) genes were concurrently found in severe congenital neutropenia patients who developed acute myeloid leukemia.21 Treatment with G-CSF and the loss of RUNX1 enhance the detachment of long-term HSCs from the niche and increase the frequency of short-term HSCs.16 We recently reported that deficiency of Runx3, a closely related member of RUNX family, also results in G-CSF hypersensitivity.22 The gene discussed is CSF3; the disease is severe congenital neutropenia.