In renal fibrosis mice, TIMAP expression was shown to be reduced, likely due to the elevated expression of TGF-β, which promoted the high expression of HDAC3 and activated the Smad signaling pathway, which combined with HDAC3 to bind near the TIMAP promoter and inhibit the expression of TIMAP, which could dephosphorylate the light chain of myosin in M2 macrophages, thereby reducing their migration and phagocytosis (Yang et al., 2017). Here, HDAC3 is linked to renal fibrosis.