On the molecular level, AAA was characterized by an early elevation of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, IL-23, MCP-1, TNFa, and IFNγ (interferon gamma)), gradual elastin and collagen degradation with further smooth muscle cell apoptosis, necrosis, and autophagy, resulted in the chronic, thrombotic process common for most human AAAs [75]. This evidence concerns the gene IFNG and achalasia-alacrima syndrome.