Our analysis also indicates down-regulation of genes involved in cell cycle (e.g., BACH1, BCL2), cytoskeletal organization (e.g., TMEM38B, SCN5A), and DNA repair pathway (e.g., SRSF657,58, DDX559, and MET60), which is consistent with our mutational signature analysis showing increased oxidative stress and defective DNA repair mechanisms in IHD cardiomyocyte. Here, BACH1 is linked to myocardial ischemia.