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. This evidence concerns the gene TGFB1 and renal fibrosis.