KRT18 and Alzheimer disease: Although we have shown in our cell model that aggregation of RD‐Tau can be induced by both synthetic K18 fibrils and natural AD‐derived fibrils, and that the resulting endogenously formed aggregates share similar kinetics of formation and cell localization, we have no formal proof that full‐length Tau aggregates induced by the presence of AD‐derived fibrils would behave the same regarding propagation, seeding, and fate in the cells.