POLA1 and dyskeratosis congenita: The pathologies associated with mutations in human CTC1 and STN1, mainly dyskeratosis congenita and Coats Plus ([72] and references therein), might therefore stem not only from deregulation in CTC1-STN1-Pol-α-telomerase interactions [73], but also from potential defects in mitotic spindle stability conferred by the mutations in S. cerevisiae CST described here.