However, since MuSK-IgG1-3 can also be detected at low concentrations in most MuSK-MG patients (67, 84), and given the evidence for complement activation in animal models (91, 92), complement inhibition may also represent a potential therapeutic approach for MuSK-MG with IgG1-3, which has not yet been validated in clinical trials. The gene discussed is MUSK; the disease is myasthenia gravis.