GP6 (glycoprotein VI) is a collagen receptor on platelets essential for hemostasis and thrombosis. Upon collagen binding, GP6 initiates platelet activation through a signaling cascade involving the FcR gamma-chain, Src kinases (FYN/LYN), SYK, the adapter protein LAT, and PLCG2 activation 1. This leads to platelet adhesion, aggregation, and procoagulant activity, ultimately promoting thrombin and fibrin formation. GP6 dysfunction contributes to bleeding disorder, platelet-type 11, while gain-of-function variants increase venous thromboembolism (VTE) risk. Genetic studies identify GP6 as a novel VTE susceptibility locus in East Asian populations, with the variant c.G1094A:p.R365H showing functional significance 2. Multiple GP6 single-nucleotide polymorphisms (rs1613662-G, rs1654419-A, rs1671153-G) associate with sticky platelet syndrome and VTE 3, and GP6 regulatory variants correlate with platelet hyperaggregability and pregnancy complications 4. Proteome-wide Mendelian randomization confirms GP6 as a causal VTE protein 1, positioning it among key therapeutic targets. Emerging evidence suggests GP6 pathway involvement in non-thrombotic conditions, including schizophrenia pathophysiology 5, indicating broader biological roles beyond hemostasis.