As RLX was also found to inhibit renal fibrosis through a TLR-4-dependent mechanism (Chen et al., 2017), which is a known inducer of the myofibroblast NLRP3 inflammasome (Boza et al., 2016), and IL-1β along with IL-18 can be produced by this inflammasome (Artlett and Thacker, 2015), we investigated whether RLX targeted TGF-β1 and TLR-4-induced NLRP3 inflammasome activity in myofibroblasts to mediate its anti-fibrotic actions. The gene discussed is TGFB1; the disease is renal fibrosis.