In a recent publication in Blood, Donini et al1 conclude that granulocyte colony-stimulating factor (G-CSF) treatment of severe congenital neutropenia (SCN) results in abnormal expression of granule-associated proteins. We have previously published this concept, 2 and showed that neutrophils from patients with SCN lack the antimicrobial peptide LL-37 and have reduced levels of defensins (HNP1–3), but are functionally capable of both phagocytosis and generating oxidative radicals. Our recent results (Figure 1) differ in part to those of Donini et al, and we would like to address this discrepancy. SCN is a heterogeneous disease that is characterized by bone marrow failure to produce normal numbers of mature neutrophils. The mechanisms behind this arrest involve apoptosis and 2 genes that are frequently mutated, HAX1 and ELA2, in autosomal recessive and autosomal dominant/sporadic SCN, respectively (reviewed in Skokowa et al4). Without correction of neutrophil levels, the patients are at risk for life-threatening infections.