Multiple mutations in known Mendelian FTD genes are described, but most of the heritability is accounted for by autosomal dominant pathogenic variation in the genes chromosome 9 open reading frame 72 (C9orf72), progranulin (GRN), and microtubule-associated protein tau (MAPT).1 Prodromal FTD presents with neuropathologic changes decades before symptoms, including brain atrophy, disrupted white matter (WM) integrity, and functional connectivity, predominantly in fronto-temporo-parietal regions.1-4. The gene discussed is MAPT; the disease is frontotemporal dementia.