For example, mutations in TERT and TERC as well as in telomere end-protective shelterins (telomeric repeat binding factor 1 [TERF1] and TRF1-interacting nuclear factor 2 [TINF2]) lead to extremely short telomeres and the development of dyskeratosis congenita and idiopathic pulmonary fibrosis, which typically present with aplastic anemia [45]. This evidence concerns the gene TERF1 and dyskeratosis congenita.