Although we did not screen the mRNA changes of all HuR targets in KH-3 treated nephritis rats, both TGFβ1 and PAI-1 among those HuR targets are well-known factors that play a critical role in the pathogenesis of organ fibrosis through stimulating matrix synthesis and accumulation and the oxidative/inflammatory insults alongside the corresponding activation of multicellular profibrotic signaling pathways. This evidence concerns the gene TGFB1 and nephritis.