Besides the known association between increased homocysteine levels and CHD risk, we found that the upregulation of MARS, caused by an increase in the MARS gene copy number in patients, was associated with the onset of CHD.[29] These phenomena associated with lysine‐homocysteinylation suggest that genetic variations of the LARS gene may contribute to K‐Leu upregulation and increased risk for CHD; these aspects warrant further studies. Here, LARS1 is linked to coronary artery disorder.