Although the mechanisms underlying the aforementioned association are not clarified, the present study proposes that a shared pathophysiological mechanism is possible for both RPL and cardiovascular disease, potentially through atheromatosis and arterial thrombosis as genetic variants of ANRIL influence atherosclerosis mechanisms such as thrombogenesis, vascular repair, and plaque stability by altering ANRIL expression and cell proliferation. Here, CDKN2B-AS1 is linked to Arterial thrombosis.