The primary molecular inhibition target of TMZ is HADHA, through which TMZ switches myocardial energy metabolism from β-oxidation of fatty acids to the faster and more efficient glucose utilization, supplying the heart with a more proficient energy turnover, making the heart more durable under conditions of energy shortage such as ischemia, diabetic cardiomyopathy or drug toxicity (Chrusciel et al. Here, HADHA is linked to ischemia.