Our recent findings revealed that RLX signaled through a RXFP1-nNOS-TLR-4-dependent mechanism in human cardiac myofibroblasts in vitro and in a murine model of isoproterenol-induced cardiomyopathy in vivo to inhibit measures of myofibroblast NLRP3 inflammasome priming and activity, as well as myofibroblast differentiation and collagen I deposition (Cáceres et al., 2019). The gene discussed is TLR4; the disease is cardiomyopathy.