Tau, a crucial neuronal protein implicated in AD, typically resides in axons under normal physiological conditions, participating in microtubule assembly.191–195 In tauopathies, it becomes hyperphosphorylated and detaches from the microtubule, exhibiting amyloid fibril characteristics.191–194,196,197 Recent studies highlight that purified full-length tau (tau441) readily undergoes LLPS in vitro, especially when crowding agents are present to mimic cellular macromolecule concentrations (Table 3). The gene discussed is MAPT; the disease is Alzheimer disease.