It is now widely accepted that the neuromuscular abnormalities in myasthenia gravis (MG) are brought about by antibody-mediated processes. A great deal has been learned about the autoantibodies against acetylcholine receptors (AChRs) and the pathogenetic mechanisms by which they produce the basic abnormalities of the neuromuscular junction in MG. However, the relationship between circulating antibodies to AChR and the severity of the disease process in myasthenic patients is highly complex. These autoantibodies are heterogeneous and differ in their ability to induce the clinical and pathophysiological features of MG. In this review, we will discuss the pathogenetic mechanisms by which AChR antibodies affect the neuromuscular junction in MG and consider how certain specijic properties of the antibodies may influence their potency. Finally, we will present new information on the apparent paradox of “antibodynegative” MG.