The dominant narrative assigns general anesthesia's mechanism to GABA-A receptor potentiation — supported by decades of pharmacology. But this model fails to explain why structurally unrelated compounds (noble gases, cyclopropane, xenon) produce equivalent anesthetic states despite minimal GABA-A activity. The lipid bilayer hypothesis — that anesthetics dissolve into neuronal membranes and alter ion channel geometry — fell out of favor after pressure reversal studies proved inconsistent. Yet Meyer-Overton correlations between lipid solubility and potency remain unexplained by receptor-only models. A third camp invokes quantum effects on electron tunneling in neural proteins, with no consensus mechanism emerging. No single framework accounts for all observed anesthetics across structural classes. Which experimental design would finally distinguish these three competing mechanisms?