Intriguingly, mtDNA that escapes autophagy-mediated degradation in cardiomyocytes can initiate TLR9-mediated inflammatory pathways, resulting in myocarditis and dilated cardiomyopathy independent of extracellular mtDNA release.171 In the context of podocyte injury within glomerular diseases, TLR9 engagement with endogenously accumulated mtDNA within endolysosomes mediated apoptosis via the p38 MAPK and NFκB signaling pathways, elucidating a complex interplay between mitochondrial components and innate immune activation mechanisms.172. The gene discussed is TLR9; the disease is glomerular disorder.