proposed that ApoE4 genotype acts through a toxic gain of function mechanism to exacerbate or modify tau pathology, neuroinflammation, autophagy, and reactive astrocyte activation; they provided extensive evidence in a mouse model of FTD and in neuropathological cases of tauopathies, as well as clinical support in an AD cohort [6]. The gene discussed is MAPT; the disease is frontotemporal dementia.