To determine whether the gene expression changes in the mouse model mimic the clinical progression of SCN to AML, we took advantage of bio-banked samples of a previously reported ELANE mutant-SCN patient who received life-long CSF3 therapy and acquired CSF3R (d715) and RUNX1 (D171N) mutations identical to our mouse model.10 The gene discussed is ELANE; the disease is severe congenital neutropenia.