Also consistent with an important role for a decline in MuSK signaling in causing aging muscle atrophy, a mouse transgenically modified to overexpress neurotrypsin [65], an endogenous protease that inactivates neural agrin [86] and thereby decreases MuSK activity [85], also causes precocious aging muscle atrophy with hallmark features we see in normally aging muscle (noted in the section “Denervation as a primary cause of sarcopenia”). This evidence concerns the gene MUSK and muscle atrophy.