This is consistent with the earlier reports of the anti-inflammatory effects of CNP and NPR-C on leukocyte trafficking.13 The parallel observations in VSMCs and macrophages reiterate the capacity of CNP to reduce several pathogenic mechanisms in the context of AA and consistent with the notion that CNP mimetics or NPR-C agonists may represent new pharmacological modalities for treating this disorder, in both TAA and AAA. This evidence concerns the gene NPR3 and triple-A syndrome.