MIF and glomerulonephritis: Endorsing our findings, Lan et al. discerned that, according to immunohistochemical analysis, MIF was a normal constituent of kidney tissues but highly upregulated in the case of glomerulonephritis, and they inferred that kidney expression of MIF was much more prominent in areas of tissue damage when compared with the histochemical appearance of other areas without damage, and they owed that to macrophage (p < 0.0001) and T cell (p < 0.05) release of MIF at areas of focal damage, not to the normally expressed MIF by glomerular or tubular cells of the kidney.