This study investigates apoptotic responses in type-I Glanzmann thrombasthenic platelets. Using washed platelets from twelve unrelated patients, calcium ionophore A23187 induced platelet activation. Flow cytometry measured phosphatidylserine exposure, Δψm depolarization, microparticle formation, and platelet shrinkage. Results showed that increased cytosolic calcium elevated PS exposure, depolarized mitochondrial potential, increased microparticle formation, and induced shrinkage. Findings indicate that GPIIb-IIIa deficiency does not limit platelet activation or apoptosis, suggesting GPIIb-IIIa-independent mechanisms contribute to normal platelet apoptosis, helping explain the normal platelet count in thrombasthenic patients.