Moreover, we previously reported that non-lesioned arteries from diabetic patients, which display relative protection from AAA development (of note, the relative contribution of hyperglycemia per se4 and metformin intake12 to AAA protection observed in diabetics remains elusive) have a distinct elevation in BM proteins lead by a 40% increase in COL4A1/A2—an observation in line with reports on increased of COL4A1/A2 in diabetic vascular organoids13 and with the well-known accumulation of BM in small vessels14. The gene discussed is COL4A1; the disease is triple-A syndrome.