In summary, based on our knowledge of the noncanonical function of TERC in the regulation of myelopoiesis, and in particular of its CR4/CR5 domain, the two aptamers that we have designed and characterized are able to perform the same function in myelopoiesis as the complete TERC molecule and to restore defective myelopoiesis in zebrafish, mouse and human models of congenital neutropenia caused by different genetic alterations, such as DC and PN. This evidence concerns the gene CRIPTOP5 and severe congenital neutropenia.