Our results demonstrate that STAT6 deletion in mice reduces the accumulation of myeloid fibroblasts and myofibroblasts, inhibits M2 macrophage polarization, and decreases the production of extracellular matrix proteins in the kidney, thereby attenuating the development of renal fibrosis and preserving renal function in folic-acid-induced nephropathy. The gene discussed is STAT6; the disease is kidney disorder.