Various in vivo experiments have shown that C/EBPα overexpression can inhibit CCl4-induced liver fibrosis [37], C/EBPβ deficiency in hematopoietic cells can mitigate bleomycin-induced pulmonary fibrosis [190], C/EBPδ lost can aggravate UUO-induced renal fibrosis [26], and C/EBPζ deficiency can alleviate TAC-induced cardiac fibrosis [311], thus providing an experimental basis for the realization of this strategy. The gene discussed is CEBPB; the disease is renal fibrosis.