Researchers reported in Nature Communications that targeted antisense oligonucleotide (ASO) therapy reversed developmental defects in spinal muscular atrophy (SMA) organoid models. The lead sentence: ASO treatment restored key developmental pathways in SMA-derived neural organoids, demonstrating a potential route to correct early neurodevelopmental deficits. The study names specific mechanisms and shows functional rescue in three‑dimensional human tissue models, offering a translational bridge between molecular correction and tissue‑level outcomes. Organoids provide a disease‑relevant platform to test sequence‑specific therapies; this work supports further preclinical development of ASOs for developmental aspects of SMA.