In the glomerulosclerosis model in vitro, BNP was shown to reduce ECM accumulation by podocytes incubated with TGFβ1, reduce TIMP2 expression and suppress glycogen synthase kinase 3 beta activity, which is closely associated with the pathogenesis of glomerulosclerosis [94] and is considered a key therapeutic target that determines the development of oxidative stress [95]. The gene discussed is GSK3B; the disease is glomerulosclerosis.