Kumar et al. reported that in rats with port-systemic shunts, the increase in skeletal muscle myostatin expression, suppressed mTORC1 function, and hyperammonemia-related stress response (i.e., autophagy markers) were reversed by ammonia-lowering therapy, concluding that it can lead to the improvement in skeletal muscle phenotype and function [128]. The gene discussed is MSTN; the disease is Hyperammonemia.