On the grounds that C5 inhibitors have already been included in the treatment routine of certain clinical and serological types of myasthenia gravis and that SELL and HLA-A may also become future potential anti-myasthenic targets, we trace the following directions for future studies: 1) to verify the function of key proteins in animal models, 2) to observe the impact on TMG prognosis after upregulating or downregulating the expression of key proteins, and 3) to explore the mechanisms of key proteins influencing the prognosis of TMG. This evidence concerns the gene SELL and myasthenia gravis.