Since oxidative stress is known to induce changes in cardiac remodeling through the development of apoptosis, necrosis, and fibrosis [13, 14], we hypothesized that treating rats with HF using the sGC stimulator (BAY41‐8543) could alleviate significant structural remodeling of the heart and, thus, at least partially contribute to the improvement of the alarmingly low survival rate (Figure 1). The gene discussed is SGCB; the disease is hydrops fetalis.