Structural synthetic lethality arises when malignant demand exceeds feasible capacity.
Unlike classical genetic synthetic lethality, it is state-dependent. It emerges in high-demand malignant regimes where compensatory options are already constrained.
Perturbation of a critical structural function under these conditions often does not produce an isolated defect. Instead, it triggers coordinated destabilization across multiple execution domains, resulting in non-compensable architectural collapse. Selectivity arises because non-malignant cells, operating under lower demand, retain sufficient architectural reserve to remain feasible.
