Furthermore, ADSC treatment effectively ameliorated diabetic nephropathy by reducing oxidative stress and inflammatory cytokines levels (e.g. IL-6 and TNF-α), by mediating the inhibition of the pro-inflammatory p38 MAPK signaling pathway (Fang et al., 2012), a factor involved in the development of human diabetic nephropathy (Adhikary et al., 2004). The gene discussed is TNF; the disease is diabetic kidney disease.