MuSK-MG patient refractoriness to, as well as the worsening of symptoms during treatment with, anti-AChE drugs [12],[32] can be attributed to: 1) Low AChE activity [30],[32]; 2) MG-induced decline of the safety factor for neuromuscular transmission [44],[77],[78]; or 3) effect of ACh dispersal on AChR clusters [49],[65]. The gene discussed is ACHE; the disease is myasthenia gravis.