It was revealed that compound 57 had the capacity to inhibit RAS and further suppress TGFβ1/Smad pathway through inhibiting Smad2/3 phosphorylation via blocking Smad2/3-TGFβRI protein interaction, and compound 57 was implicated in activation of RAS/TGFβ1/Smad axis in HK-2 cells and podocytes, indicating that compound 57 played a beneficial role in renal fibrosis and podocyte injury and could be considered as a novel RAS inhibitor for treating CKD (Wang et al., 2017). Here, SMAD2 is linked to chronic kidney disease.