C9orf72 and frontotemporal dementia: Belzil and collaborators reported that reduced C9ORF72 expression in the frontal cortex and cerebellum from C9-ALS and C9-FTD patients was associated with increased binding of C9ORF72 to repressive histone methylation marks, namely H3K9me3, H3K27me3, H3K79me3, and H4K20me3 [115], providing a second mechanism for gene silencing in addition to the aforementioned DNA methylation and highlighting again the beneficial effect of epigenetic methylation reaction in silencing the toxic repeat expansions of C9ORF72 [115].