Moreover, Rac1-MR activation and inflammation in the kidney of high-salt-fed DS rats were ameliorated by BPS treatment, which suggested that inflammation-induced Rac1-MR pathway activation is involved in the progression of salt-induced kidney injury and that BPS treatment suppresses renal inflammation, leading to the attenuation of Rac1-MR activation and kidney damage (Figure 5). This evidence concerns the gene NR3C2 and Dravet syndrome.