Since DOCA/salt treatment (Lother et al., 2016; Cao et al., 2019) as well as genetic deletion of the natriuretic peptide receptor GC-A (Kuhn et al., 2002; Kilic et al., 2005; Nakagawa et al., 2016) not only result in renal damage but also in cardiac hypertrophy and fibrosis, expression levels of marker genes for hypertrophy (BNP) and fibrosis (α-smooth muscle actin, TGF-β, collagen types 1 and 3) were determined in the respective models. The gene discussed is TGFB1; the disease is cardiac hypertrophy.