In particular, we investigated the extent to which (1) RXFP1, AT2R, P2X7R, TLR-4, ROS (which is another trigger of NLRP3 inflammasome activity) and caspase-1 were involved in the NLRP3 inflammasome-inhibitory effects of RLX in HCMFs in vitro; and (2) the P2X7R was involved in the NLRP3-inhibitory, anti-fibrotic and cardioprotective effects of RLX, in mice with cardiomyopathy in vivo. This evidence concerns the gene TLR4 and cardiomyopathy.