The clinical and immunological heterogeneity that characterizes myasthenia gravis (MG) has implications for etiology, pathogenetic mechanisms, cellular interactions, and treatment. Moreover, it raises the important question of whether MG is a “single” disorder, attributable exclusively to autoantibodies directed against the postsynaptic nicotinic acetylcholine receptor (AChR). In this paper we present evidence that antibodies to determinants other than AChR may impair neuromuscular transmission in some MG patients, show data indicating a diversity of genetic factors influencing susceptibility to MG, and describe recent immunohistological and functional studies of the thymus and of thymic cells.