For example, studies from large genetic FTD‐centered initiatives have shown that GFAP is only elevated in familial FTD due to progranulin (GRN) mutations,37 which is a TDP43 proteinopathy, and similarly, that NfL levels have different trajectories over time, with faster increases in GRN mutation carriers.40 This evidence concerns the gene GRN and proteostasis deficiencies.