Stress testing is performed in experimental contexts that preserve the execution demands characteristic of advanced malignancy, including sustained proliferation, elevated biosynthetic throughput, coordinated trafficking, and heightened mitotic activity.
Under these conditions, perturbations are evaluated by their capacity to compromise cell-wide coordination. Local disruptions that remain confined to a single execution domain and fail to propagate across domains are not considered evidence of architectural dependence. Discovery under oncogenic load therefore prioritizes feasibility loss over pathway modulation.
