TRMT5 and hereditary spastic paraplegia: The mutation of TRMT5 in humans abolishes its function to methylate tRNA at G37 and causes a series of diseases, such as hereditary spastic paraparesis [78], neuropathy syndrome [79], combined oxidative phosphorylation deficiency 26 (COXPD26) [80], idiopathic non-cirrhotic portal hypertension, and hepatopulmonary syndrome [81], etc., which are associated with the impaired translation efficiency and fidelity in mitochondrial proteins that depend on the correct methylation of mt-tRNA m1G37 by TRMT5.