Importantly, the CR4/CR5 domain of TERC is essential for performing this novel role in the regulation of myelopoiesis, since a mutation of this domain found in dyskeratosis congenita (DC) patients, but not patient mutations affecting other domains, results in the inability of TERC to properly regulate myelopoiesis and to physically interact with RNA Pol II, despite its DNA binding capacity being unaffected9. This evidence concerns the gene CRIPTOP5 and dyskeratosis congenita.