LCN2 and triple-A syndrome: For instance, it has neutrophil-chemotactic properties, and neutrophil infiltration is a well-recognized mechanism of tissue injury in the setting of AAA.28,29 In addition, LCN2 has been shown to augment endoplasmic reticulum stress and inhibits reparative autophagy in SMCs and cardiomyocytes respectively,30–32 and autophagy is recognized as a reparative mechanism that maintains tissue integrity in the setting of AAA.33,34 Our data confirmed that LCN2 is present in the aneurysm tissue of AAA patients, showing some colocalization with the peripheral neutrophil marker Ly6g+Lyc6 (Figure S2B).