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However, clinical translation remains constrained by its reliance on supra\u2010clinical irradiation doses. Here, we present a unifying framework redefining RDDS through two distinct paradigms: structural disassembly and molecular actuation. We delineate their radiochemical foundations, highlighting reductive and electron\u2010driven mechanisms as more robust and tumor\u2010selective than stochastic reactive oxygen species\u2010mediated pathways. Furthermore, we position radiation\u2010driven gas therapy as a distinct modality based on in situ molecular generation. Critically, we identify the dose\u2013response mismatch between radiolytic chemistry and clinical radiation as the central translational bottleneck. To overcome this, we propose a design paradigm centered on highly predictable, dose\u2010matched activation, where mechanisms directly coupling radiation energy to molecular transformation offer superior predictability. 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