However, the cardioprotective effects associated with Bach1 deficiency in mice also appear to be partially mediated by activation of the STAT3 pathway and by the inhibition of p38/MAPK signaling and apoptosis [22], and Bach1 deficiency reduces the proliferation of SMCs as well as neointimal formation in a murine model of arteriosclerosis via an HO-1-independent mechanism [30]. This evidence concerns the gene BACH1 and arteriosclerosis disorder.