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While gene\u2010directed modalities, specifically viral\u2010mediated supplementation, antisense oligonucleotides (ASOs), and CRISPR\u2010based activation or precision editing, offer a means to rescue loss\u2010of\u2010function phenotypes, successful clinical implementation requires moving past the reductive framework of merely increasing the expression of the target gene towards approaches that account for spatial, developmental, and therapeutic windows. This review uses HNRNPU\u2010related rare neurodevelopmental disorder (HNRNPU\u2010RNDD), a condition marked with global developmental delay and refractory epilepsy, as an exemplar to discuss these translational hurdles. We discuss the homeostatic boundaries of this scaffold attachment factor, where unregulated overexpression risks localised cytotoxicity, and altered chromatin dynamics compromise editing safety. Furthermore, we assess how cell\u2010type sensitivity and narrow developmental windows may dictate clinical efficacy. 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