Inflammation contributes to tubular atrophy and interstitial fibrosis.[9] Macrophages are one of the primary cell types recruited during tubulointerstitial fibrosis.[11] The recruitment of macrophages may contribute to kidney repair at the early stages, but this repair can ultimately cause renal fibrosis.[10, 11] Regardless, ablation studies show that macrophages play important roles in stimulating fibrosis.[32] In our study, HO-1 overexpression obviously inhibited the infiltration of macrophages at every time point following UUO. The gene discussed is HMOX1; the disease is renal fibrosis.