Upregulation of osteoprotegerin (member of the cytokine receptor of tumour necrosis factor (TNF) receptor superfamily) in human AAA biopsies promoted an inflammatory vSMC phenotype with impaired proliferation and increased apoptosis.47, 48 Oxidative stress is another driver for the switch from contractile to synthetic phenotype.39, 41 Furthermore, the Notch1 pathway is known to be involved in AAA formation and vSMC‐specific haploinsufficiency of Notch1 maintains the contractile vSMC phenotype and prevents matrix remodelling in the murine abdominal aorta.43 The gene discussed is TNFRSF11B; the disease is triple-A syndrome.