Therefore, to clarify whether the antioxidative effects of sesn2 were protective against LPS treatment, we examined (i) whether sesn2 knockdown decreased AMPK phosphorylation, (ii) whether sesn2 knockdown regulated ROS production and antioxidant gene expression, (iii) whether sesn2 knockdown regulated the expression of apoptosis-related molecules and cardiomyocyte death, and (iv) whether sesn2 knockdown increased cardiomyopathy-related factors (e.g., MMP2, MMP9, collagen I, and collagen III) upon LPS-induced inflammation in H9c2 rat cardiomyocytes and heart tissue obtained from C57BL/6 mice. The gene discussed is PRKAB1; the disease is cardiomyopathy.