This dissertation proposal investigates the impact of HbS (sickle cell hemoglobin) binding to GP1bα on platelet activation in patients with sickle cell disease (SCD). The proposal includes an introduction to SCD, its global prevalence, and the role of platelet activation in the disease's pathology. It reviews existing literature on the genetic basis of SCD, the function of hemoglobin, and the relationship between platelet activation and vascular complications. The research aims to determine if GP1bα binding to HbS leads to platelet activation in SCD patients, potentially contributing to intravascular clot formation. The proposed methodology involves collecting blood samples from SCD patients and healthy controls, with specific inclusion and exclusion criteria. Ethical considerations are addressed, including informed consent and patient confidentiality. The proposal outlines a timeline for the research and includes a comprehensive list of references. The expected outcome is a better understanding of the mechanisms driving platelet activation in SCD, which could inform the development of targeted therapies to prevent vascular complications.