Acquired platelet function disorders (PFDs) are rare conditions characterized, in most cases, by reduced platelet function and bleeding symptoms. Among acquired PFDs with a bleeding phenotype, drug-induced PFDs are the most common and can often be suspected and diagnosed based on a history of recent platelet-inhibiting drug administration. Less commonly, acquired PFDs are caused by autoimmune mechanisms. Diagnosis in these cases can be particularly challenging. In fact, demonstrating the presence of autoantibodies that inhibit platelet function is often difficult, especially in centers without specific expertise in complex platelet disorders. Among autoimmune PFDs (aPFDs), acquired Glanzmann thrombasthenia (aGT), is the most common. It is caused by autoantibodies that bind to the platelet αIIbβ3 integrin, thereby inhibiting its function. Autoimmune GT can be associated with underlying hematological malignancies or autoimmune diseases but it can also be idiopathic. More rarely, other immune-mediated PFDs can occur, such as acquired delta storage pool disease (aδSPD). Autoimmune PFDs should be suspected in patients with unexplained mucocutaneous bleeding of recent onset, no previous history of hemorrhage, normal coagulation tests and platelet count, and no use of platelet-inhibiting medications. The concomitant presence of underlying diseases associated with autoantibody production further suggests an immune-based PFD. Symptoms can range from mild to severe mucocutaneous bleeding. The treatment of aPFDs must focus on the control of acute bleeding, on administration of immunosuppressive treatment to reduce or eliminate autoantibodies, and on management of the underlying disease in secondary forms. When associated with another condition, aPFDs may completely resolve upon treatment of the underlying disease. In most cases of primary and secondary aPFDs, immunosuppressive therapies can lead to complete or partial remission of the bleeding.