To minimize the side effects, specific strategies were developed to suppress pathogenic macrophage infiltration, polarization, and myofibroblast transition via chemokines (CCL2, CCL5, CXCL16, and CCL21) and their receptors, Src, JAK-STAT, and TGFβ1/Smad3 signaling inhibition, respectively, to attenuate the progression of renal fibrosis. The gene discussed is CCL2; the disease is renal fibrosis.