By exploiting TGF-β-stimulated fibroblast NRK-49 F cells to simulate renal fibrosis, Yang et al. reported that HG was able to inhibit the proliferation and fibrosis of NRK-49 F cells, decrease the expression of α-SMA, collagen I, and collagen III, and downregulate the level of phosphorylated Smad2/3 through suppressing the activity of the M3 receptor (Yang and He, 2022). Here, ACTA1 is linked to renal fibrosis.