In this context, the hormone relaxin, known as anti-fibrotic agent and under clinical investigation in heart failure patients (Moin et al., 2016), was shown to inhibit the TGF-β1/Smad3 axis and to counteract TGF-β1-induced transition of neonatal cardiac stromal cells and NIH3T3 fibroblasts to myofibroblasts acting via the up-regulation of Notch1 signaling (Sassoli et al., 2013; Squecco et al., 2015; Zhou et al., 2015). The gene discussed is TGFB1; the disease is heart failure.