Conversely, a very recent study reported that tumor necrosis factor receptor-associated factor-2 (TRAF2), an innate immunity effector, is essential for physiological mitophagy in cardiomyocytes, since its myocardial loss (in inducible cardiac-myocyte specific TRAF2 knockout mice) impairs physiological mitophagy in the heart inducing cardiac inflammation, thus supporting a cardioprotective role of TRAF2-stimulated mitophagy [108]. This evidence concerns the gene TRAF2 and inflammatory response.