Similarly, decreased H3K9me3 mark was associated with the pathological findings in C9orf72 BAC transgenic mice [168], suggesting the contribution of SUV39H1/2, a histone lysine methyltransferase or Kdm4d demethylase (demethylates H3K9me3) responsible for H3K9me3 mark, in the pathophysiology of ALS. This evidence concerns the gene C9orf72 and amyotrophic lateral sclerosis.