Platelet adhesive protein defects are a significant subset of inherited platelet function disorders that impair platelet adhesion, aggregation, and hemostasis, leading to bleeding diathesis. These defects primarily involve mutations in key glycoprotein receptors such as GPIb-IX-V, αIIbβ3, GPVI, α2β1, and GPIV. These conditions include Bernard-Soulier syndrome (BSS), platelet-type von Willebrand disease (PT-VWD), 22q11.2 microdeletion syndrome, Glanzmann thrombasthenia (GT), αIIbβ3-related thrombocytopenia, and collagen receptor defects. Recent advances in molecular genetics, especially next-generation sequencing, have contributed to the identification of the underlying genetic mutations, offering deeper insights into their pathophysiological mechanisms. The chapter describes the pathogenetic mechanisms of these disorders, their genetic bases, and the associated clinical manifestations and underscores the importance of accurate laboratory diagnosis. Further investigation into the molecular mechanisms of these diseases will be essential to unravel disease heterogeneity and improve patient management.