Although tempting to employ AAT-KO mice as a categorical control group, we wish to note that such animals exhibit the phenotype of AAT-deficient individuals (excess neutrophilic activity, widespread vasculitis and, depending on the engineered mouse line, aggregate-burdened hepatocytes); we do not assume a surgical cut has an underlying lack of AAT levels, but rather that elevated AAT provides benefit, and further so when it is a form that negates cleavage by target proteases—the only process that literally cuts short the half-life of native AAT. Here, SERPINA1 is linked to vasculitis.