AARS1 and peripheral neuropathy: In spite of the possible contribution of mitochondrial toxicity induced by PN-GlyRS variants [44], the cytosolic toxicity induced by tRNAGly sequestration is likely a critical contributor to peripheral neuropathy phenotypes, because (i) in PN-GlyRS mouse models, transgenic tRNAGly overexpression fully rescues peripheral neuropathy phenotypes [12], and (ii) all of the seven other PN-associated aaRS genes exclusively encode the cytosolic aaRS, with the corresponding mitochondrial aaRSs being encoded by different genes.