Additionally, the global deletion of BACH1 in mice has been shown to reduce atherosclerosis progression through the upregulation of HO‐1 expression, a known protective mechanism against oxidative stress.[127] Therefore, there are at least two mechanisms for BACH1 deficiency to alleviate atherosclerotic lesion formation: firstly, it can have an anti‐inflammatory impact by suppressing YAP activation in ECs, and secondly, it can produce anti‐oxidative effects dependent on HO‐1. This evidence concerns the gene BACH1 and atherosclerosis.