Using the human aorta database, we identified putative signaling pathways that could be potentially regulated by H3 modifications during AAA formation (e.g., PI3K-Akt pathway, endocytosis, actin cytoskeleton, focal adhesion for H3K4me1 and calcium signaling, glutamatergic synapse, cholinergic synapse, associated with H3K9me3). The gene discussed is AKT1; the disease is triple-A syndrome.