Childhood Obstructive Sleep Apnea Contributes to a Leading Health Burden

associated with IPF as an epiphenomenon or whether they are causative. Genetic data suggest the latter. Multiple rare mutations in the genes that encode both the protein and RNA components of telomerase have been found in families and in sporadic individuals with IPF and other ILD subtypes (3, 4). The heterozygous missense mutations in genomic DNA are not induced by lung disease and have been present since birth. Most of these mutations create an enzyme complex that has less than 100% activity in in vitro assays, and all are associated with short telomere lengths of circulating leukocytes, even for many younger individuals in the families who are not affected with pulmonary fibrosis (1). Prospective follow-up of these individuals over time will be important to reveal the true incidence of pulmonary fibrosis in this cohort with genetically determined short telomere lengths.