In studies conducted on a mouse model, the authors demonstrated that the deficiency or inhibition of the NF-κB (p50) subunit by decoy oligonucleotides or anti-NF-κB agents inhibited the formation and progression of intracranial aneurysms and suppressed the expression and production of pro-inflammatory proteins crucial to their development, such as MCP-1, interleukins, and extracellular matrix metalloproteinases29,32. Here, CCL2 is linked to Dilatation of the cerebral artery.