MuSK MG is phenotypically different from classic AChR-antibody-mediated MG by a more frequent presentation of bulbar weakness, less responsiveness to symptomatic therapy with acetylcholinesterase inhibitors, the absence of a thymoma, and a better therapeutic response to a cluster of differentiation (CD-20) B-cell therapy such as rituximab. This evidence concerns the gene ACHE and myasthenia gravis.