Telomere biology disorders (TBDs) are caused by impaired telomere maintenance. Critically short telomeres limit the replicative cell capacity, leading to reduced tissue renewal. TBDs are characterized by cancer predisposition and multiorgan system complications, including organ failure and/or fibrosis. Progressive bone marrow failure (BMF) is the most common life-threatening complication, affecting up to 80% of patients with dyskeratosis congenita (DC). Classical DC is caused by autosomal and X-linked mutations on telomere maintenance-associated genes. The curative treatment for the BMF of these patients is bone marrow transplantation. However, the poor outcomes of transplanted patients make necessary the development of alternative therapies. To evaluate the efficacy of lentiviral vectors expressing DKC1 and TERC genes to keep telomere homeostasis, we first generated gene-edited CD34⁺ cells harboring DKC1 and TERC recognized mutations (DC-like CD34⁺ cells). Thereafter, telomere length and expansion rates were then evaluated ex vivo, either on untransduced and transduced DC-like CD34⁺ cells. Compared to healthy CD34⁺, DC-like CD34⁺ cells showed accelerated telomere attrition. Remarkably, transduction with the respective therapeutic vectors restored telomere length dynamic, as well as the ex vivo expansion of DC-like progenitor cells. Our next steps will consist of efficacy evaluation of lentiviral-mediated gene therapy in DC-like CD34⁺ cells after transplantation into immunodeficient mice. Additionally, gene therapy will be tested in lymphoblastic cell lines and hematopoietic stem cells from DC patients. These results initiate a pathway for building strategies to be used as alternative therapies for DC patients.