Consequently, these data suggest that in the present study and, thus, in the context of a CKD rat model, elevated Npp3 and Npp1 expression, rather than Tnap, might be responsible for the hydrolysis of PPi into Pi in the aortic tissue and, by these means, the stimulation of the arterial calcification process. The gene discussed is ENPP1; the disease is chronic kidney disease.