Furthermore, animal experiments have determined that mucins secreted by cancer cells trigger the reciprocal activation of PLTs and NEs, leading to the formation of microthromboembolism.[13] Consistent with earlier findings, our study demonstrated that GCS patients had significantly elevated CA125 levels when compared to GC patients, and a multivariate logistic regression analysis revealed that these elevated CA125 levels independently increased the risk of stroke in GC patients. The gene discussed is MUC16; the disease is stroke disorder.