Missense mutations in a short stretch of amino acids of TIN2 (the DC patch) are responsible for ~25% of DC cases (Savage et al., 2008; Walne et al., 2008; reviewed in Savage and Bertuch, 2010), whereas the majority of DC cases are due to mutations impinging on telomerase biogenesis and activity. Here, TINF2 is linked to dyskeratosis congenita.