Myasthenia gravis (MG) is an acquired antibody-mediated autoimmune disease of the neuromuscular junction. The pathophysiology is widely studied and overall well understood. In MG, the binding of antibodies with nicotinic acetylcholine receptor (AChR) and other proteins (e.g., muscle-specific kinase, MuSK) to the postsynaptic membrane result in decreased binding of Ach to the receptors and increased destruction of the receptors. There are several other antibodies found in patients with MG such as lipoprotein-related protein 4 antibodies (LRP4), titin antibodies, ryanodine receptor antibodies (RyR), and voltage-gated potassium channel antibodies (VGKC); however, their prevalence is relatively low and their sensitivity and specificity to MG is still under study. Thymic lymphofolliculuar hyperplasia is common in patients with MG (70%); however, thymic tumor (thymoma) is only seen in 10% of patients. Symptoms present more commonly in women in their 20s and 30s and in men in their 50s and 60s, with overall higher prevalence in women.