The following results support our conclusion: (i) results from BM transplantation experiments verify that BM-derived FSP-1+ cells are involved in the process of developing renal inflammation and fibrosis; (ii) specifically blockades of Notch/RBP-Jκ signaling in FSP-1+ cells inhibit macrophage infiltration and renal fibrosis in UUO; (iii) the secretion of cytokines and chemokines from activated BM-derived FSP-1+ cells is suppressed by KO of RBP-Jκ. The gene discussed is RBPJ; the disease is renal fibrosis.