This discrepancy likely reflects the distinct genetic backgrounds: the C57BL/6 wild-type mice represent a relatively normal state in which DKK3 deficiency alone may cause baseline hypertension, whereas Apoe−/− mice inherently exhibit marked dyslipidemia and spontaneous endothelial dysfunction/susceptibility to atherosclerosis, creating a pro-hypertensive milieu that may mask or alter the specific contribution of Dkk3 deficiency to baseline BP regulation [69,70]. Here, APOE is linked to atherosclerosis.