Lately, with the aim of delineating the intricate molecular background of these effects, Shen et al. highlighted that the improvement of LV function, alongside the reduction in sympathetic activity, is driven by repressing BACH1 and PACS-2-mediated mitochondrial oxidative stress by inactivating the TGF-β1/SMADs/SP1 pathway in a rat model of HF, expanding our understanding of the cellular-level benefits of SNS blockade in HF models [96]. The gene discussed is SP1; the disease is hydrops fetalis.