TRMT61B and inborn mitochondrial metabolism disorder: Interestingly, overexpression of TRMT61B, the methylase for m1A (Chujo and Suzuki 2012), restored not only m1A levels, but also mitochondrial translation levels, without altering the steady-state level of mt-tRNALys (Richter et al. 2018); however, before we can consider the potential application of TRMT61B overexpression to other mitochondrial diseases, we must elucidate how overexpression of TRMT61B promotes mitochondrial translation.