The functional autoantibodies have provided new insights into potential pathophysiologic mechanisms in numerous autoimmune diseases. Early detection of these autoantibodies and their removal by immunotherapy offers an additional approach to treatment that may halt disease progression and prevent the chronic irreversible changes that are typical of autoimmune disease. There is likely to be a large family of functional autoantibodies. The earliest functional autoantibodies detected in the neurologic diseases myasthenia gravis, Lambert-Eaton myasthenic syndrome (LEMS), and neuromyotonia, have their parallel in naturally occurring genetic disorders affecting the skeletal muscle nicotinic receptor, P/Q-type voltage-gated calcium channels (VGCCs), and voltage-gated potassium channels (VGKCs). It seems more than reasonable to assume that autoimmune equivalents can also be detected for diseases affecting other ion channels or receptors. It is noted that a better understanding of these autoantibodies is likely to enhance greatly our ability to diagnose, monitor, and treat the associated autoimmune diseases.