FGFBP1 and neuromuscular disease: For example, FGFBP1 is secreted from muscle fibres during denervation and is particularly important for NMJ maintenance during aging and ALS.41, 42 Interestingly, approaches targeting neuromuscular diseases like ALS or SBMA with mTORC1 inhibitors, like rapamycin, to activate autophagy in motor neurons, have proven detrimental for disease progression.11, 12 It is possible that the unexpected negative effect of rapamycin treatment in these pathologies is due to its negative effect on NMJ maintenance by the muscle fibres.