Moreover, the calcium content in the thoracic aorta correlated positively and significantly with Enpp1 and Enpp3 aortic mRNA gene expression in vehicle-treated CKD rats and, as such, can be seen as (1) a survival mechanism, increasing local PPi levels to target the present arterial calcifications, or perhaps (2) an adverse process, by depleting local ATP levels leading to less purinergic signaling. Here, ENPP3 is linked to chronic kidney disease.