Abs in patients with MG are against the muscle nicotinic acetylcholine receptor (AChR), muscle-specific tyrosine kinase (MuSK), and lipoprotein-related protein 4 [1, 3, 5, 7], and are secreted by B cells and plasma cells with assistance from CD4+ T cells [1, 8], resulting in complement anti-AChR antibodies damaging the neuromuscular junctions and inducing MG symptoms such as ptosis, dysphagia, limb weakness, and even dyspnea [4, 9]. This evidence concerns the gene CD4 and myasthenia gravis.