Furthermore, considering that TIMP-3 has been validated as a target of miR-181b,13 our experiments conducted in Timp3–deficient mice strongly imply that the beneficial effects afforded by miR-181b inhibition are largely TIMP-3 dependent during atherosclerosis in Apoe−/− mice, although an additional protective effect is achieved through elevating elastin synthesis during formation of AAAs. The gene discussed is APOE; the disease is achalasia-alacrima syndrome.