Hypoxia triggers activation of platelets, leading to thrombosis. If not addressed clinically, it can cause severe complications and fatal consequences. The current treatment regime for thrombosis is often palliative and include long-term administration of anticoagulants, causing over-bleeding risk and other secondary effects as well. This demands a molecular understanding of the process and exploration of an alternative therapeutic avenue. Interestingly, recent studies demonstrate that platelets exhibit functional autophagy. This cellular homeostatic process though well-studied in non-platelet cells, is under-explored in platelets. Herein, we report autophagy activation under physiologically relevant hypoxic condition (10% O