Since lupus nephritis is pathologically characterized by the deposition of the ICs in glomeruli, we speculate that the mtDNA in the ICs may be transported to podocytes through endocytosis and then either reach endolysosomes to activate the de novo expressed TLR9 or act on NLRP3/inflammasomes, resulting in podocyte injury/apoptosis and IFN-α and proinflammatory IL-1 production thereby facilitating LN development. This evidence concerns the gene TLR9 and lobular neoplasia.