PARN (poly(A)-specific ribonuclease) is a 3'-5' exoribonuclease that preferentially degrades poly(A) tails of mRNAs, serving as a critical deadenylase in eukaryotic cells 1. Its primary function involves catalyzing deadenylation, the initial and rate-limiting step in mRNA decay 1. PARN operates through a mechanism requiring interaction with both the 3' poly(A) tail and 5' cap structure for efficient degradation, and participates in nonsense-mediated mRNA decay, AU-rich element (ARE)-containing mRNA degradation, and microRNA processing 2. Beyond mRNA regulation, PARN functions in non-coding RNA maturation, telomere biology, oocyte maturation, and embryogenesis 1. Recent evidence demonstrates PARN's role in miRNA biogenesis, including trimming of miR-451 intermediate forms to mature length 3, and in maintaining stability of H/ACA box snoRNAs 2. Clinically, pathogenic PARN variants cause dyskeratosis congenita and telomere-related bone marrow failure syndromes 2, 4. PARN mutations appear in approximately 30% of familial interstitial lung disease cases and are associated with accelerated disease progression 4. Deregulated PARN activity has been implicated in various cancers and inherited bone marrow failure syndromes 1. The gene's multifaceted roles in RNA metabolism and telomere maintenance underscore its importance in maintaining genomic stability and preventing age-related diseases.