Gene silencing of c-Myc reversed the increased expression of PCNA and the ECM proteins and also blocked or attenuated the antifibrotic effect of SSR in IL-1β-induced NRK-49F cell, suggesting that c-Myc is involved in the progression of RIF and is an important target for SSR in the improvement of renal fibrosis. The gene discussed is IL1B; the disease is renal fibrosis.