Additionally, we have demonstrated that the CR4/CR5 domain is indispensable for this novel, noncanonical function of TERC, since a TERC molecule harboring a mutation in the CR4/CR5 domain found in DC patients is unable to regulate the expression of myeloid genes, whereas mutations of DC patients in other domains do not affect this function. The gene discussed is TERC; the disease is dyskeratosis congenita.