The pathogenesis of MG involves an autoimmune response targeting components of the neuromuscular junction (NMJ), where nerve impulses trigger muscle contractions. MG is primarily driven by an autoimmune response, where the body's immune system mistakenly identifies components of the NMJ as foreign and attacks them. The primary target of this autoimmune response is the AChRs on the muscle cell membrane. These receptors normally bind acetylcholine, a neurotransmitter released by motor neurons, to initiate muscle contractions. In MG, the immune system produces autoantibodies called anti-AChR antibodies. These antibodies bind to the AChR on the muscle cell membrane, leading to several effects: (i) some antibodies block the binding sites on the AChR, preventing acetylcholine from binding and initiating muscle contractions; (ii) other antibodies may cross-link adjacent AChR molecules, leading to internalization and degradation of the AChR complex, reducing the number of functional receptors on the muscle cell membrane; (iii) the binding of antibodies to AChR can also activate the complement system, a part of the immune system involved in inflammation and cell destruction. This further contributes to damage and dysfunction at the NMJ. The presence of anti-AChR antibodies and complement activation disrupts neuromuscular transmission, leading to: (i) reduced signal transmission, since with fewer functional AChR available, the binding of acetylcholine released by motor neurons is impaired, resulting in weakened muscle contractions; (ii) endplate destruction, since chronic immune-mediated damage to the NMJ can lead to structural changes, including destruction of the postsynaptic membrane and alterations in the distribution of AChR. The thymus gland plays a role in the development of MG in some individuals. It is commonly associated with thymic abnormalities, such as thymic hyperplasia or thymoma (a tumor of the thymus). The thymus is thought to contribute to the production of autoantibodies and the maturation of autoreactive T cells involved in the autoimmune response seen in MG. In general, the pathogenesis of MG involves a complex interplay between autoantibodies, complement activation, and immune-mediated damage at the neuromuscular junction, leading to impaired neuromuscular transmission and muscle weakness characteristic of the disease. Genetic background of myasthenia gravis Myasthenia gravis has a complex genetic background, but it is not typically considered a purely genetic disorder like some other conditions. Instead, MG is primarily regarded as an autoimmune disease with genetic predispositions. While the exact cause of MG is unknown, there is evidence suggesting a genetic predisposition to the disease. Certain genetic variations or polymorphisms have been associated with an increased risk of developing MG. These variations are often related to genes involved in immune system function, such as genes encoding human leukocyte antigens (HLAs), specifically the HLA-B8 and HLA-DR3 alleles. MG can sometimes run in families, indicating a potential genetic component. Family studies have shown that first-degree relatives of individuals with MG have a higher risk of developing the condition compared to the general population. However, the inheritance pattern is usually not straightforward, suggesting the involvement of multiple genetic and environmental factors. Certain HLA alleles, particularly those within the major histocompatibility complex (MHC) region, have been consistently linked to an increased risk of MG. For example, the HLA-DR3 allele has been associated with MG, especially in individuals with early-onset disease and thymic abnormalities. 332 However, HLA associations alone are not sufficient to explain the development of MG, indicating the involvement of other genetic and environmental factors. In addition to HLA alleles, studies have identified other genetic factors that may contribute to the risk of MG. These include genes involved in immune regulation, such as those encoding cytokines, chemokines, and components of the complement system. Variations in these genes may affect immune function and predispose individuals to autoimmune diseases like MG. Using data from the CAS Content Collection, we have put together genes known to have an association with MG (Figure ). These genes include AGRN, LRP4, MUSK, and TTN. A comprehensive table, including extensive details regarding genes, related proteins, expression profiles, function, and other diseases, as well as multiple examples, is included in the Supporting Information, Table )