In the context of diabetes, adverse cardiac remodelling was abrogated by Rac1 deletion in cardiomyocytes leading to less NOX2 activation and PERK/ATF-6 induced ER stress.93 In a rabbit model of myocardial infarction, remote myocardial NOX2 expression was found to be increased, in association with increased oxidative stress, elevated C/EBP homologous protein (CHOP), and cleaved ATF6. Here, DDIT3 is linked to diabetes mellitus.