The SNPs that did not reach HW equilibrium in our cohort of patients with a clinical diagnosis of FTD were located in genes associated with AD and PSP (APOE, CR1, MS4A6A, and STX6 genes), which can be explained due to the sample size, or because these genes are subject to selection with each other between FTD and other neurodegenerative diseases (12, 37). Here, STX6 is linked to Alzheimer disease.