We assume that low expression of serum NLRC5 may contribute little to the deposition of NLRC5 in the kidneys but may serve as a trigger for inflammatory reaction in IgAN, local production of NLRC5 by endothelial cells, dendritic cells, and macrophages in the kidneys might be the main source of local NLRC5 deposition because of the local inflammatory response in IgAN, as NLRC5 promotes proinflammatory responses in parenchymal cells in acute renal failure (AKI) [16] and in mesangial cells in diabetic nephropathy (DN) [34], beyond the regulation of MHC class I genes. This evidence concerns the gene NLRC5 and liver dysplastic nodule.