In our study on the rat model of T1DM, the NO-independent chronic activation of sGC by cinaciguat effectively restores glomerular cGMP levels, and attenuates diabetic podocyte damage, glomerular apoptosis and fibrosis through suppression of TGF-ß overproduction and ERK1/2 phosphorylation. This evidence concerns the gene MAPK3 and type 1 diabetes mellitus.