The literature has previously reported on innovative renoprotective interventions exploiting macrophage polarization as a way to condition the ECM at the site of injury and effect an antifibrotic outcome.99 Some of the most notable work in this field has been done by Harris and colleagues, wherein splenic macrophages were modified ex vivo with IL-10/TGF-β to induce or polarize to an anti-inflammatory, antifibrotic M2 phenotype.100 These M2s were then transfused into a mouse with Adriamycin nephropathy, a condition considered analogous to human focal segmental glomerulosclerosis. Here, TGFB1 is linked to focal segmental glomerulosclerosis.