The disrupted LRP4-MuSK interaction was also shown to correlate with a lack of the compensatory presynaptic increase of released acetylcholine vesicles (i.e., quantal content, QC) in in vivo models of MuSK-MG, which, by contrast, is commonly observed in AChR-MG disease models and in patient muscles (75–77). This evidence concerns the gene MUSK and myasthenia gravis.