Additionally, activation of signaling pathways such as mTOR, JAK/STAT, TGF-β/Smad, smooth muscle-enriched Nox4, and SMARCD1 promotes VSMC inflammation and aneurysm progression, whereas pathways including PPARγ, RhoGAP, and Nrf2-Keap1 attenuate the pro-inflammatory VSMC phenotype, thereby mitigating vascular inflammation and preventing AAA development [17,75,77,78]. The gene discussed is TGFB1; the disease is triple-A syndrome.