The comment by Burgod et al.,1 for which we are grateful, encompasses invaluable insights on the use of gene expression as a disease stratification tool in neonatal encephalopathy (NE). Its main drawbacks are depicted, and interesting alternatives are suggested. In the present letter, we aim to provide an accurate reply to their concerns, which we read with the utmost attention.

In the first place, we must apologize for not citing the article by Montaldo et al.2,3 The first draft of our manuscript4 was written long before it was sent to consideration for publication, and we made the tremendous mistake of not updating the whole cited literature in the very final version. During this time, Montaldo et al. published a study of gene expression profiling in infants with NE.2,3 As per our knowledge at the time, we wrongly claimed that ours was the first study of this kind. We thank Burgod and their team for giving us the opportunity to publicly amend this mistake, and it is with pleasure that we rectify ourselves. In their study, Montaldo and colleagues identified 950 statistically significant genes discriminating between healthy controls and newborn infants with NE. The main pathways involved in NE were axonal guidance signaling, granulocyte adhesion and diapedesis, IL-12 signaling and production in macrophages, and hypoxia-inducible factor 1α signaling. Only 137 genes were shared between NE-affected babies and septic babies. The authors concluded that gene expression profiles could ease disease stratification and personalized neuroprotective therapies.2

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