Further studies demonstrated that the protective effect of WA against the GalN/LPS-induced FH was partially dependent on NLRP3 inflammasome antagonism in vivo and has a direct anti-inflammatory influence partially dependent on the presence of NLRP3 in macrophage in vitro, indicating that other targets, beyond NLRP3, mediate the anti-inflammatory effect of WA. The gene discussed is GAL; the disease is familial hyperaldosteronism.