Research found that compared to wild-type mice and mice with single knockout of either GSDMD or GSDME, double knockout of GSDMD and GSDME conferred enhanced protection against FA-AKI modeling, attenuating NET formation, macrophage polarization, and subsequent renal fibrosis development (148), an effect likely attributable to the concurrent blockade of GSDME-mediated RTECs pyroptosis within the inflammatory milieu together with GSDMD-mediated NET release and the subsequent NET-driven macrophage-to-myofibroblast transition (MMT). The gene discussed is GSDME; the disease is Friedreich ataxia.