It was recently demonstrated that RLX was able to suppress TGF-β1-induced myofibroblast differentiation and interstitial collagen (collagen I) deposition through a RXFP1-nNOS-TLR-4-NLRP3 inflammasome-dependent mechanism in human cardiac myofibroblasts (HCMFs) and the left ventricle of mice with cardiomyopathy, leading to the amelioration of the pro-fibrotic influence of the TGF-β1/IL-1β and TGF-β1/IL-18 axes on cardiac fibrosis progression [34] (Figure 1). Here, NLRP3 is linked to cardiomyopathy.