In human brain microvascular endothelial cells and mouse brain microvessels, the pro-inflammatory cytokine Tnf-α dramatically increases Icam1 mRNA and protein levels by regulating H3K9me2, which is achieved by treatments with histone methyltransferase G9a and demethylase Kdm4b. Moreover, G9a overexpression or Icam1 or Kdm4b depletion reduces inflammation-induced leukocyte extravasation, which indicates that blocking Icam1 or Kdm4b may offer a novel therapeutic approach for treating brain diseases [134]. This evidence concerns the gene ICAM1 and brain disorder.