We recently demonstrated in TGF-β1-stimulated human cardiac myofibroblasts in vitro and in the left ventricle of mice subjected to isoproterenol-induced cardiomyopathy in vivo that RLX could inhibit the TGF-β1/IL-1β/IL-18 axis via a RXFP1-nNOS-TLR-4-NLRP3 inflammasome-dependent mechanism (Cáceres et al., 2019). The gene discussed is NLRP3; the disease is cardiomyopathy.