Therefore, a vicious circle involving slanDCs, bacterial LPS, TNFα and CX3CL1 could maintain the chronic inflammation that is associated to aneurysm progression, where slanDCs would favor TNFα-mediated CX3CL1 production, which in turn would promote slanDC and other CX3CR1+ inflammatory cell recruitment, all together leading to both ATLO formation and aneurysm progression. The gene discussed is CX3CR1; the disease is aneurysm.